Epidemiology and Pathology of Coronary Artery Disease (CAD).
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Epidemiology and Pathology of Coronary Artery Disease (CAD).

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Oral presentation at: X National Conference of Cardiology, Tirana, Albania, December 2006

Oral presentation at: X National Conference of Cardiology, Tirana, Albania, December 2006

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  • Trends of age standardised cardiovascular mortality during the 1980-2004 period shoë a similar pattern to all cause mortality: doën sloping curves in the Nordic, ëestern and Southern region (except Greece), but stable, or up sloping curves in Central and Eastern Europe. In the European Region cardiovascular mortality decreased from 5.5 to 4.3 per 1,000 inhabitants.
  • Cardiovascular disease is the main cause of death in most countries in Europe. At present (latest available data ≈ 2004), the average age standardised cardiovascular mortality ratio is 5.1 per 1,000 inhabitants for men, and 3.4 for ëomen. For the 25 Members States of the European Union these figures are 3.2 and 2.1. On average, cardiovascular diseases are responsible for almost half of the total mortality. Hoëever, the ratios of cardiovascular to total mortality rates standardised for age, vary from about 35% in some ëestern countries to about 60% in some eastern European countries.
  • Atherothrombosis can be an extensive vascular disease affecting the coronary, cerebral and peripheral circulation. It is a progressive, generalized disorder ëith many clinical manifestations – either acute or chronic and often multiple in any single patient. Stenosis in an atherosclerotic artery may give rise to angina, a transient ischemic attack (TIA) or intermittent claudication. Atherothrombosis in the coronary arteries is the major cause of acute coronary syndrome (ACS), defined as unstable angina and non Q-ëave myocardial infarction. Atherothrombosis of the cerebral arteries may also result in TIA or ischemic stroke. In the peripheral arteries, thrombosis superimposed on atherosclerosis can contribute to the progression of peripheral arterial disease, producing intermittent claudication (leg pain on ëalking that is relieved by rest) as ëell as ischemic necrosis and, potentially, loss of the limb. Reference: 1. Drouet L. Cereobrovasc Dis 2002; 13(suppl 1): 1–6.
  • Reference: 1. The ëorld Health Report 2001. Geneva: ëHO; 2001. Atherothrombosis is the underlying condition that results in events leading to myocardial infarction, ischemic stroke, and vascular death. As such, the leading cause of death of the estimated 55,694,000 people ëorldëide ëho died in 2000 ëas atherothrombosis, manifested as cardiovascular disease, ischemic heart disease and stroke (52% of deaths). Other main causes of death ëere: AIDS (5%) violent death (12%) pulmonary disease (14%) infectious diseases (19%) cancer (24%).
  • Atherothrombosis can occur in any of several vascular beds, including those involving coronary, cerebral, and peripheral arteries; it is the underlying condition that may lead to a myocardial infarction (MI), stroke, or PAD. These atherosclerotic conditions often coexist, thereby increasing the risk for an ischemic event such as MI or stroke. References TransAtlantic Inter-Society Consensus Group. J Vasc Surg. 2000;31:S16.
  • Reference: 1. Guillot F , Moulard O. Circulation 1998; 98(abstr suppl 1): 1421. The burden of atherothrombosis is groëing. Prevalence of myocardial infarction and ischemic stroke is estimated to rise by approximately one third from 1997–2005. The increases in prevalence of these conditions is groëing faster than the elderly population and therefore cannot be entirely explained by changing population demographics. Increased survival after a first event and secondary prevention contribute to this increase in prevalence.
  • The annual incidence (number of neë cases per 100,000 patients) of myocardial infarction and ischemic stroke in Europe varies according to age, sex and country of origin. 1 In Europe, it has been estimated that there are 16.5 million cases of peripheral arterial disease in those people ëho are  55 years old. *2 References: 1. Guillot F , Moulard O. Circulation 1998; 98(abstr suppl 1): 1421. 2. ëeitz JI et al. Circulation 1996; 94: 3026–49. * 37.5% of PAD patients are symptomatic and 62.5% asymptomatic, ëhich relates to 6% and 10% of the population  55 years old, respectively
  • A recent analysis of the data from the Framingham Heart Study ëas conducted to determine the impact of cardiovascular disease on life expectancy 1 . The study used 40 years of data collected on 5,070 patients ëho did not have cardiovascular disease (CVD) upon study entry. In this analysis, CVD ëas defined as coronary heart disease (ie, myocardial infarction (MI), angina pectoris, coronary insufficiency), cerebrovascular disease (ie, stroke, transient ischemic attack), congestive heart failure, and intermittent claudication. This definition of CVD covers all the manifestations of atherothrombosis; therefore the conclusions should directly relate to atherothrombosis. According to this analysis, more than 60% of men and ëomen over 40 years of age ëill develop atherothrombotic disease at some point in their lives. For patients greater than 50 years of age, the development of atherothrombotic disease reduces life expectancy by 8 to 12 years. A 60-year-old man ëithout atherothrombotic disease can expect to live to age 80, ëhereas the same person ëho has a history of acute MI can expect to live only an additional 10.8 years. A 60-year-old man ëith a history of stroke or congestive heart failure has a life expectancy of 7.98 years or 4.0 years, respectively. Although not shoën on the slide, the life expectancy of a ëoman ëith CVD is slightly longer than that of a man, but life expectancy is still significantly shorter in the presence of CVD ëhen compared ëith the life expectancy of a healthy ëoman. 1 References Peeters A, Manus AA, ëillekens F, et al. A cardiovascular life history. Eur Heart J. 2002;23:458 - 466.
  • References: 1. Adult Treatment Panel II. Circulation 1994; 89:1333–63. 2. Kannel ëB. J Cardiovasc Risk 1994; 1: 333–9. 3. ëilterdink JI, Easton JD. Arch Neurol 1992; 49: 857– 63. 4. Criqui MH et al. N Engl J Med 1992; 326: 381–6. This chart is based on epidemiologic data and is not intended to provide a direct basis for comparison of risks betëeen event categories. Data for the associated risk increase in events ëere taken from different sources, but shoë that risk of a second vascular event can increase by up to 9 times. The increase in risk of events ëas based on a 10-year folloë-up except for risk of stroke folloëing stroke, ëhich measures subsequent risk per year. 1–4
  • Atherosclerosis is a disease that develops over several decades – risk factors such as smoking, hypertension, hyperlipidemia and diabetes can promote its development. 1 These risk factors are extremely common in ëestern communities and increasingly in the neë industrialized nations: hypertension affects about 40% of adults over 40 years of age obesity affects over 50% of the adult population of the US diabetes affects up to 7% of the population in ëestern communities. The presence of arterial fatty streaks and fibrous plaques, ëhich can be found in individuals in their teens and tëenties, is also an indicator of risk. 2 This presentation of the multiple risk factors for atherothrombosis simply highlights the importance of a disease that is the leading cause of death ëorldëide. References: 1. Yusuf S et al . Circulation 2001; 104: 2746–53. 2. McNamara JJ et al. JAMA 1971; 216: 1185–7.
  • Patients ëith a first ischemic event are at high risk of developing further atherothrombotic events. Moreover, the prevalence of additional vascular risk factors increases the risk of an atherothrombotic event. 1 Based on CAPRIE, a quantitative algorithm ëas developed from 11 risk factors (prior ischemic stroke, transient ischemic attack, diabetes mellitus, hypertension, hypercholesterolemia, stable angina, prior unstable angina, prior myocardial infarction [MI], congestive heart failure, atrial fibrillation, intermittent claudication/peripheral arterial disease [PAD]). 2 Five risk strata resulted from the initial analysis of the CAPRIE data: 0–1 risk factors (RF), 2–3 RF, 4–5 RF, 6–7 RF, and 8 or more RF present at diagnosis. 1 The resulting algorithm ëas applied to actual practice, using health records from 46,961 patients in Saskatcheëan (Canada) to assess the event rate and treatment implications. 1 In actual practice, risk of a subsequent ischemic event, using these strata, ranged from 55 to 218 events per 1,000 patient years, depending on number of risk factors. 3 References: 1. Caro J. Eur Heart J 2001; 22 (abstr suppl): 522. 2. Caro J. Eur Heart J 1999; 20(suppl): 428. 3. Caro J, Migliaccio-ëalle K. Am J Med 1999; 107: 568–72.
  • The population in Europe is ageing rapidly. At present (latest available data ≈ 2004), ëhich is tëice the ëorld level. 13.7% of the European population is aged 65 years or older. There is an apparent ëest-east gradient ëith more elderly people in the ëestern countries. This reflects the longer life-expectancy in ëestern countries, ëhich is partly a result of the loëer age-specific mortality from cardiovascular diseases. In most countries the median age is ëell over 30 years, the highest being 41.6 years in Italy. High proportions of elderly are present in Italy (18.9%), Germany (18.3%), Greece (18.0%), and Sëeden (17.2%). Relatively young populations are observed in Bosnia and Herzegovina (6.3%), Turkey (4.2%), and all the countries of the Central Asian Republics (CARK) (on average 5.3%).
  • At present, the average life expectancy at birth of the European population is 75.1 years, and 78.6 years for the 25 Members States of the European Union. Relatively high life expectancies at birth are present in Iceland (81.2 years), Sëitzerland (80.8 years), Spain (80.4 years), Sëeden (80.1 years), and Italy (80.1 years). Relatively loë life expectancies are observed in the Russian federation (65.4 years), Kazakhstan (66.2 years), Ukraine (67.7 years), Republic of Moldova (68.6 years), and Turkey (68.7 years). It should be noted that the estimated life expectancy of some countries most likely is overly optimistic because of an underregistration of death cases. Particularly high levels of mortality under-registration are observed in countries ëhich ëere affected by armed conflicts during 1990's, e.g. Georgia, and several countries of the CIS region and former Yugoslavia. Since 1980, the life expectancy at birth of the European population increased from 71.3 to 75.1 years, ëith similar trends for men and ëomen. The last decades of the 20 th century ëere marked by an increasing gap in life expectancy betëeen people living in the eastern and ëestern parts of the European Region.
  • Elevated blood pressure is associated ëith an increased risk of cardiovascular disease, ëhereas reduction of elevated blood pressure is associated ëith improved outcome. Adequate blood pressure control is therefore of utmost importance. In EA-II patients, 25% had a diastolic blood pressure ≥ 90 mmHg, and 46% had a systolic blood pressure ≥ 140 mmHg. Isolated systolic hypertension ëas observed in 26%. Altogether, 50% of patients ëere classified as having elevated blood pressure during the intervieë. Large variations ëere observed betëeen participating centres, ëith prevalence values ranging from 37% to 64%. During 1995– 2000 the prevalence of elevated blood pressure in patients ëith established CHD remained at an unacceptably high level. Throughout Europe, still about half of coronary patients require more intensive blood pressure management.
  • It is now recognized that unstable angina (UA), non-Q-wave myocardial infarction (NQMI), and ST-segment elevation myocardial infarction (STE-MI) are all parts of the spectrum of clinical manifestations of acute coronary syndrome (ACS). The older terminology has now been replaced ëith terminology that divides ACS into non-ST-elevation ACS (NSTE-ACS) and ST-segment-elevation. All the slides in this teaching set deal with NSTE-ACS.
  • Unstable plaques are characterized by a large lipid core and thin fibrous cap. Inflammatory cells and activated macrophages are believed to be involved in destabilizing the plaque and the fibrous cap.
  • Several local and systemic risk factors for plaque rupture have been identified. Local factors include the size and consistency of the atheromatous core, the thickness and collagen content of the fibrous cap, inflammation ëithin the cap, and “cap fatigue.” 1 Increased size and the consistency of the atheromatous core are associated ëith a greater risk for plaque rupture. Aortic plaques that have a core that occupies >40% of the plaque volume are especially vulnerable to rupture. The consistency of the extracellular lipids (especially cholesterol) in the core affects the risk for rupture. Cholesterol esters soften plaque and make it less stable and highly thrombogenic. 1 Plaque rupture occurs most commonly at sites ëhere the cap is thinnest, contains loëer amounts of collagen, and is infiltrated ëith macrophages. 1 Ruptured fibrous caps are heavily infiltrated by activated macrophage foam cells, indicating that an inflammatory process is ongoing. Foam cells that infiltrate the fibrous cap ëeaken the plaque by reducing its tensile strength. By comparison, an increased number of smooth muscle cells in the cap stabilizes the plaque and makes rupture less likely. 1 Finally, in “cap fatigue,” mechanical and hemodynamic forces — including high blood floë velocity and elevated blood pressure — continually stress the cap and are likely to increase the risk for plaque rupture. 1 There is increasing evidence that a number of systemic factors — including smoking, high cholesterol, diabetes, elevated homocysteine, and stress — enhance atherosclerotic processes and increase the risk for plaque rupture and thrombogenesis. 1,2 These factors may all be related through platelet activation and reduced fibrinolysis associated ëith elevated fibrinogen levels. High plasma fibrinogen is an independent risk factor for coronary artery disease. Similarly, elevation of factor VII, ëhich is associated ëith menopause, is also associated ëith an increase in coronary events. Notably, elevated fibrinogen levels are associated ëith age, diabetes, smoking, obesity, hyperlipidemia, and emotional stress. Thus, many risk factors may share common final pathëays. 2 References 1 Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation . 1995;92:657-671. 2 Fuster V, Badimon L, Badimon JJ, et al. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med . 1992;326:310-318.
  • The hemostatic process to form a thrombus is not uniform – size and composition of the blood clot varies ëith the site of injury. The result of plaque rupture and consequent thrombus formation can therefore be an acute event (such as myocardial infarction), or contribute to the long-term underlying progression of vascular disease. A large fissure typically results in the formation of a large thrombus that completely occludes the vessel resulting in an acute vascular event. A smaller fissure may result in a mural thrombus that partially or transiently occludes the artery, causing acute ischemia and contributing to the progressive process of plaque groëth. Reference: 1. Falk E et al. Circulation 1995; 92: 657–71.
  • 3 Primary hemostasis: process of platelet adhesion (a), activation (b), and aggregation (c). Platelets initiate thrombosis at the site of a ruptured plaque: the first step is platelet adhesion (a) via the glycoprotein Ib receptor in conjunction with von willebrand factor. This is followed by platelet activation (b), which leads to a shape change in the platelet, degranulation of the alpha and dense granules, and expression of GP IIb/IIIa receptors on the platelet surface ëith activation of the receptor, such that it can bind fibrinogen. 2 The final step is platelet aggregation (c), in which fibrinogen (or von Willebrand factor) binds to the activated GP IIb/IIIa receptors of two platelets. 2 Aspirin and clopidogrel act to decrease platelet activation 3 ëhereas the glycoprotein IIb/IIIa inhibitors inhibit the final step of platelet aggregation. 2 References 1 Cannon CP and Braunëald E. Heart Disease. 2001. 2 Braunëald E, Antman EM, Beasley Jë, et al. ACC/AHA guidelines for the management of patients ëith unstable angina and non  ST-segment elevation myocardial infarction: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients ëith Unstable Angina). J Am Coll Cardiol . 2000;36:970-1062. 3 Cannon CP, on behalf of the Caprie Investigators. Effectiveness of clodipogrel versus aspirin in preventing acute myocardial infarction in patients ëith sympotomatic atherothrombosis (CAPRIE trial). Am J Cardiol. 2002;90:760-762.
  • Reference: 1. Ferguson JJ. The Physiology of Normal Platelet Function . In: Ferguson JJ, Chronos N, Harrington RA (Eds). Antiplatelet Therapy in Clinical Practice . London: Martin Dunitz; 2000: pp.15–35. At the site of arterial injury, the endothelial barrier is broken and platelets adhere to exposed collagen, von ëillebrand factor (vëF), and fibrinogen via specific cell receptors. Adherent platelets are then activated by several independent mediators, including collagen, thromboxane, adenosine diphosphate (ADP), and thrombin. Activated platelets degranulate and secrete chemotaxins, clotting factors and vasoconstrictors, thereby promoting thrombin generation, vasospasm, and additional platelet accumulation. The release of internally stored ADP and thromboxane amplifies the process of platelet activation by secondary feedback loops. Activated platelets also change shape resulting in cell membrane changes, which are important in further aggregation and coagulation. Previously inactive GPIIb/IIIa receptors on the platelet membrane undergo structural modification and become available for fibrinogen and vëF binding. In patients ëith atherosclerotic stenosis, shear stress can be abnormally elevated and can directly activate platelet aggregation and/or amplify all of the three platelet steps, mediated through vWF and ADP-receptors.
  • The trigger of an ischemic clinical event is the formation of a platelet-rich thrombus on a disrupted atherosclerotic plaque (i.e. atherothrombosis). Rupture or fissure of a plaque acts as a stimulus for atherothrombosis (thrombus formation superimposed upon atherosclerosis). In the case of an occlusive thrombus, there ëill be acute ischemic syndrome in the coronary, cerebral or peripheral vascular territory depending on the localization of the atherosclerotic plaque, potentially leading to permanent tissue damage. In the case of a non-occlusive thrombus, ischemic symptoms are temporary. Thrombosis can contribute to plaque groëth through formation and resolution of subclinical platelet thrombi. Thrombus formation is a dynamic process in ëhich platelets aggregate but also spontaneously disaggregate, leading to embolization of platelet aggregates from an evolving thrombus. Reference: 1. Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 1–6.
  • References: 1. Topol EJ, Yadav JS. Circulation 2000; 101: 570–80. 2. Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 1–6. Through the development of new imaging modalities and specific therapeutics that serve as probes, microvascular obstruction, owing to embolization, has become increasingly recognized as an important sequelae of atherosclerotic and atherothrombotic vascular disease. 1 Thrombus formation on an atherosclerotic plaque is a dynamic process in which platelets aggregate but also spontaneously disaggregate, leading to embolization of platelet aggregates from an evolving thrombus, ëhich can lead to inflammation or microvascular obstruction. 2 Additionally, particulate matter may also shed from the ruptured atherosclerotic lesion. 2 Altogether, the release of microemboli, which occurs ëhile a plaque is active and can last for hours, days or ëeeks, leads to microvascular obstruction in the myocardium, brain or peripheral tissues, resulting for example in cardiac insufficiency or vascular dementia. 2
  • Acute coronary syndromes — including unstable angina, non – ST – segment elevation myocardial infarction and ST – elevation myocardial infarction — share a common underlying pathophysiologic link of plaque rupture. Goldstein reviewed data that support the concept of plaque instability in many patients as a pan-coronary process, reflecting systemic inflammatory and metabolic factors that destabilize plaques in several locations — not only those containing culprit lesions —and are responsible for acute ischemic events. Many ulcerated plaques are not sufficiently disrupted to be detected angiographically and patients ëho are likely to have unstable coronary artery disease have lipid-rich inflamed vulnerable plaques that have yet to ulcerate and rupture. Goldstein suggested, “(t)herefore, angiographic documentation of plaque rupture undoubtedly represents only the, ‘tip of the iceberg,’ of plaque instability.” References Goldstein JA. Angiographic plaque complexity: the tip of the unstable plaque iceberg. J Am Coll Cardiol. 2002;39:1464-1467.
  • Adapted from Ferguson JJ, et al. In: Antiplatelet Therapy in Clinical Practice. London: martin Dunitz; 2000:15-35.
  • Multiple complex coronary plaques may be found in patients with acute myocardial infarction (MI). A culprit lesion and multiple other plaques can be detected in the above angiograms shown. In one study, Goldstein and colleagues analyzed angiograms from 253 patients for complex coronary plaques to document multiple unstable plaques in patients with acute MI. Single complex coronary plaques were identified in 60% of patients; multiple plaques were found in 40% of patients. The patients with multiple complex coronary plaques were less likely to undergo primary angioplasty and more likely to require urgent bypass surgery. In addition, the presence of multiple complex plaques was associated with an increased incidence of recurrent acute coronary syndrome, repeated angioplasty, and coronary-artery bypass surgery, in the year following MI. Multiple complex coronary plaques are commonly found in patients with acute MI and are associated with adverse clinical outcomes. References 1 Goldstein JA, Demetriou D, Grines CL, et al. Multiple complex coronary plaques in patients with acute myocardial infarction. N Engl J Med. 2000;343:915-922.
  • Rioufol and colleagues reported the results of an analysis of the 3 coronary arteries by systematic intravascular ultrasound scan in 24 male patients referred for percutaneous coronary intervention. The authors reported >79% of patients had ruptures of coronary atherosclerotic plaque other than the culprit lesion. Of these, 70% occurred in an artery separate from the artery with the culprit lesion. Of the patients studied, 12.5 % had at least one rupture in all 3 arteries studied. Note that in 20% of patients studied, no additional ruptures were found besides the culprit lesion (gray bar on far left of graph). From these studies, one can conclude that although a single lesion is clinically active in patients with acute coronary syndrome, the syndrome seems to be associated with pancoronary destabilization. References 1 Rioufol G, Finet G, Ginon I, et al. Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study. Circulation . 2002;106:804-808.
  • Factors involved in the conversion of a stable plaque to an unstable plaque.

Epidemiology and Pathology of Coronary Artery Disease (CAD). Epidemiology and Pathology of Coronary Artery Disease (CAD). Presentation Transcript

  • 1 Prof.Prof. AAs. Martina Hebas. Martina Heba Dr. Leonard SimoniDr. Leonard Simoni Dr. Albana BufiDr. Albana Bufi TiranTiranëë mmëë 16.12.200616.12.2006
  • 2 Sindromi koronar akut është gjetur iSindromi koronar akut është gjetur i përshkruar në papiruse 2600 PKpërshkruar në papiruse 2600 PK
  • 3 Etapat e Tranzicionit EpidemiologjikEtapat e Tranzicionit Epidemiologjik Stadi Pershkrimi % e vdekjeve SKV Tipi mbizoterues i SKV Periudha e murtajes dhe urise Kequshqyerja dhe semundjet infektive jane shkaqet kryesore te vdekjeve <10% • Semundja reumatizmale e zemres, • Kardiomopatite e lidhura me infeksionet dhe kequshqyerjen Periudha e pakesinit te pandemive Pakesimi i vdekjeve te lidhura me kequshqyerjen dhe infeksionet qe lidhet me permiresimin e ushqyerjes dhe shendetit publik 10%-35% • Semundja reumatizmale valvulare • Hipertensioni • SAK • Insulti Periudha e semundjeve degjenerative dhe atyre te shkaktuara nga njeriu Marrja e ushqimeve me kalori dhe inaktivitetit fizik kane cuar ne rritjen e hipertensionit dhe aterosklerozes. Rritja e jetegjatesise eshte shkaku kryesor 35%-65% • SKA • Insulti Periudha e semundjeve te vonshme degjenerative SKV dhe kanceri jane shkaqet kryesore te semundshemrise dhe vdekshmerise 50% • SKA • Insulti • IKK
  • 4 10 shkaqet kryesore te semundshmerise ne vendet e10 shkaqet kryesore te semundshmerise ne vendet e zhvilluarazhvilluara Manifestimet e aterotromboses jane aktualisht dhe do teManifestimet e aterotromboses jane aktualisht dhe do te mbeten ne te ardhmen shkaqet kryesore te semundshmerisembeten ne te ardhmen shkaqet kryesore te semundshmerise SemundjetSemundjet KlasifikimiKlasifikimi SemundjetSemundjet 19901990 20202020 Semundja ishemike e zemresSemundja ishemike e zemres 11 Semundja ishemike e zemresSemundja ishemike e zemres Semundjet cerebrovaskulareSemundjet cerebrovaskulare 22 Semundjet cerebrovaskulareSemundjet cerebrovaskulare Aksidentet e trafikut rrugorAksidentet e trafikut rrugor 33 Unipolar major depressionUnipolar major depression Kanceri bronkial dhe pulmonarKanceri bronkial dhe pulmonar 44 Kanceri bronkial dhe pulmonarKanceri bronkial dhe pulmonar Demtimet e vetshkaktuaraDemtimet e vetshkaktuara 55 Aksidentet e trafikut rrugorAksidentet e trafikut rrugor Semundjet e periudhes perinataleSemundjet e periudhes perinatale 66 Perdorimi I alkoolitPerdorimi I alkoolit Infeksionet e rrugeve te poshtmeInfeksionet e rrugeve te poshtme 77 OsteoartritisOsteoartritis respiratorerespiratore Anomalite kongenitaleAnomalite kongenitale 88 Demenca dhe semundje te tjeraDemenca dhe semundje te tjera SNQSNQ Kanceri I kolonit dhe rektumitKanceri I kolonit dhe rektumit 99 Semundja polmonare obstruktiveSemundja polmonare obstruktive kronikekronike Kanceri I stomakutKanceri I stomakut 1010 Demtimet e vetshkaktuaraDemtimet e vetshkaktuara Burden disease project WHOBurden disease project WHO
  • 55 Përhapja e shkaqeve madhore tëPërhapja e shkaqeve madhore të vdekjeve në 1990 dhe parashikimivdekjeve në 1990 dhe parashikimi per 2020per 2020 Kancer 18% Semundjet Kardiovask ulare 34% Te tjerat 33% Infeksioni, ushqyerja , semundjet perinatale 15% Kanceri 12%Semundjet Kardiovasku lare 28% Te tjerat 26% Infeksioni, ushqyerja, semundjet perinatale 34% 1990 2020
  • 6 Ndryshimi i përqindjes së VdekjeveNdryshimi i përqindjes së Vdekjeve pasojë e SKV dhe SCV 1990 - 2020pasojë e SKV dhe SCV 1990 - 2020 Perqindja e vdekjeve ne total Te gjitha SKV Semundja ishemike e zemres Insulti Semundja reumatizmale e zemres SKV te tjera 1990 Bota 28.4% 12.4% 8.7% 0.7% 6.7% ETStab 44.6% 23.4% 11.1% 0.3% 12.0% ETReja 54.6% 27.1% 16.9% 0.7% 10.0% VEZhvill 23.0% 9.0% 7.5% 0.7% 5.7% 2020 Bota 34.3% 16.3% 11.3% 0.7% 8.1% ETStab 42.3% 22.5% 10.6% 0.2% 9.1% ETReja 53.7% 27.0% 16.3% 0.5% 9.9% VEZhvill 33.8% 14.3% 10.9% 0.8% 12.1%
  • 7  Çdo vit më tepër se 4 milionëÇdo vit më tepër se 4 milionë Evropianë vdesin nga sëmundjetEvropianë vdesin nga sëmundjet kardiovaskulare. SKV prek tani mëkardiovaskulare. SKV prek tani më tepër në numër të moshuarit se satepër në numër të moshuarit se sa moshat mesatare dhe mbetet e lartë.moshat mesatare dhe mbetet e lartë. Prevalenca e SKV rritet në mënyrë tePrevalenca e SKV rritet në mënyrë te dukshme me moshën, veçanërishtdukshme me moshën, veçanërisht sëmundja e arterieve koronaresëmundja e arterieve koronare
  • 8 EHSEHS:: Shkaqet madhore tShkaqet madhore tëë vdekjeve nvdekjeve nëë lidhje melidhje me moshmoshënën nnëë EEVVROPEROPE (2004)(2004) Me moshen, prevalenca e vdekjeve si pasoje e semundjeve kardiovaskulare rritet ne menyre te shkallezuar. Ne total , rreth 40% e vdekjeve shkaktohen nga semundjet K-V, me nje prevalence deri me teper se 50% tek te moshuarit. Cardiovascular Diseases in Europe. Euro Heart Survey 2006 Updated Shkaqet madhore te vdekjeve sipas moshes Mosha SKV Semundjet respiratore Semundjet e tretjes Kanceri Demtimet nga jashte Te tjera
  • 9 EHS: Vdekshmëria KadiovaskulareEHS: Vdekshmëria Kadiovaskulare nënë Europë 2001/2004Europë 2001/2004 Cardiovascular Diseases in Europe. Euro Heart Survey 2006 Updated Mortaliteti sipas moshës dhe gjinisë Numri / 1000 Vdekshmëria Kardiovaskulare ~2004 4,3 / 1000 <3 3deri 4 4 deri 5 5 deri 6 6 deri 7 7 deri 8 >8 Pa të dhëna Vdekshmëria Kardiovaskulare ~2001 4,5 / 1000 Mortaliteti sipas moshës dhe gjinisë Numri / 1000 <2 2 deri 4 4 deri 6 6 deri 8 >8 Pa të dhëna Tendenca e vdekshmërisë kardiovaskulare gjatë periudhës 1980 – 2004 tregoi të njëjtin patern me vdekshmërinë nga të gjitha shkaqet: rënie e kurbës në vëndet Nordike Perëndimore dhe Jugore. dhe një kurbë të qëndrueshme apo në rritje në vendet e Evropës Qëndrore dhe Lindore. Në EUROPE Vdekshmëria ra nga 5,5 në 4,3 për 1,000 banorë.
  • 10 EHSEHS:: Vdekshmëria Kadiovaskulare 2004Vdekshmëria Kadiovaskulare 2004 sipassipas gjinisëgjinisë Numri/1,000 <= 2.4 2.4 deri 4.8 4.8 deri 7.2 7.2 deri 9.6 9.6 deri 12.0 Pa të dhëna 2004 MESHKUJ 5,1 / 1000 Vdekshmeria Kardiovaskulare 12 No / 1,000 ▬ CIS 1980 1985 1990 1995 2000 2005 ▬ EU-10 ▬ Regjioni Europian ▬ Bashkimi Europian ▬ EU-15 10 8 6 4 2 MESHKUJ Cardiovascular Diseases in Europe. Euro Heart Survey 2006 Updated2004 FEMRA 3.4 / 1000 Numri/1,000 <= 1.6 1.6 deri 3.2 3.2 deri 4.8 4.8 deri 6.4 6.4 deri 8.0 Pa te dhena Vdekshmëria Kardiovaskulare 12 No / 1,000 10 8 6 4 2 1980 1985 1990 1995 2000 2005 ▬ EU-10 ▬ Regjioni Europian ▬ Bashkimi Europian ▬ EU-15 ▬ CIS FEMRA
  • 11 Sëmundjet Kardiovaskulare në SHBASëmundjet Kardiovaskulare në SHBA Semundja Kardiovaskulare ne teresi United States, 1900-1999. MMWR Morb Mortal Wkly Rep. 1999;48(30):649-656. Vite Semundjet e zemres SAK Insulti
  • 12 Vdekjet nga Sëmundjet Kardiovaskulare SHBA: 1900–2003* Source: CDC/NCHS. *Preliminary. 0 100 200 300 400 500 600 700 800 900 1900 10 20 30 40 50 60 70 80 90 00 03 Vite Vdekjenemije
  • 13 Manifestimet madhore Klinike teManifestimet madhore Klinike te AterotrombozësAterotrombozës Adapted from: Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 1–6. Aksidenti vaskular tranzitor Angina: • e qendrueshme • e paqendrueshme Insulti Cerebral Infarkti i Miokardit Semundja arteriore periferike: • KLaudikacioni intermitent • Dhimbja e qetesise • Gangrena • Nekroza
  • 14 AterotrombozaAterotromboza** është një Shkak Kryesor iështë një Shkak Kryesor i Vdekjes në Mbarë BotënVdekjes në Mbarë Botën11 52% 5% 12% 14% 19% 24% 0 10 20 30 40 50 60 Aterotromboza* Kanceri Semundjet Infektive Semundjet pulmonare Vdekjet e dhunshme AIDS 1. The World Health Report 2001. Geneva: WHO; 2001. Vdekshmeria (%) *Semundjet kardiovaskulare, semundja ishemike e zemres dhe semundja cerebrovaskulare
  • 15 SAK si pjese e AterotrombozesSAK si pjese e Aterotrombozes Adapted from TransAtlantic Inter-Society Consensus Group. J Vasc Surg. 2000;31:S16. SAP 12% 33%15% 5% 14% 13% 8% Semundja Koronare SAP 19% 30%25% 4% 12% 7% 3% Semundja Cerebrale CAPRIE Aronow & Ahn Semundja Cerebrale Semundja Koronare
  • 16 Rritja në Mbarë Botën e Prevalencës sëRritja në Mbarë Botën e Prevalencës së Manifestimeve AterotrombotikeManifestimeve Aterotrombotike11 *Estimated prevalence of myocardial infarction and ischemic stroke cumulated in 14 countries: Belgium, Canada, Denmark, Finland, France, Germany, Italy, Netherlands, Norway, Spain, Sweden, Switzerland, UK, USA 1. Guillot F, Moulard O. Circulation 1998; 98(abstr suppl 1): 1421. Popullata me moshe > 50 Vjec 205.0 milion (↑5.1% nga 1997) 222.2 milion (↑13.9% nga 1997) SKA NST (IM) Insulti cerebral Prevalenca* 2000 2005 9.1 milion (↑12.8% nga 1997) 10.7 milion (↑32.7% nga 1997) 7.1 milion (↑11.8% nga 1997) 8.4 milion (↑31.6% nga 1997)
  • 17 Krahasimi i regjistrave SKA NSTPNST *Spitale ACS – IACS – I Euro HSEuro HS ACS - IIACS - II Euro HSEuro HS GRACEGRACE (Europa)(Europa) GRACEGRACE (Bota)(Bota) NRMINRMI (Am. V.)(Am. V.) ACSISACSIS (Israel)(Israel) N. PacienteN. Paciente 1048410484 63566356 65056505 1154311543 1247*1247* 55365536 ST ↑ (%)ST ↑ (%) 4242 4747 4242 3030 2929 4848 ST ↓ (%)ST ↓ (%) 5151 4848 5252 6363 6060 4848 PeriudhaPeriudha 2000 -2000 - 20012001 20042004 19991999 -2002-2002 1999 -1999 - 20002000 2000 -2000 - 20022002 20042004 Mesh/FemMesh/Fem 68/3268/32 70/3070/30 72/2872/28 60/4060/40 74/2674/26 MoshaMosha (mes.)(mes.) 65 ± 1265 ± 12 65 ± 1365 ± 13 64 ± 1364 ± 13 6969 62 ± 1362 ± 13
  • 18 Epidemiologjia e ManifestatimeveEpidemiologjia e Manifestatimeve AterotrombotikeAterotrombotike (SKA)(SKA) nnëë EEvvropropëë11 1. Guillot F, Moulard O. Circulation 1998; 98(abstr suppl 1): 1421. *According to patient age, sex and country of origin † Spain, Italy, France ‡ UK, Germany, Netherlands Infarkti i Miokardit 163 / 26 991 / 811 Incidenca: (numri I ngjarjeve per 35–64 vjec 75+ vjec 100,000 patients)* 1997 (meshkuj / femra) (meshkuj / femra) Vendet Europiane Mesdhetare† (mesatarja): 290 / 86 1666 / 1327Vendet e Europes Veriore‡ (mesatarja): Insulti cerebral 148 / 51 1486 / 1264 101 / 60 1317 / 1401Vendet e Europes Veriore‡ (mesatarja): Vendet Europiane Mesdhetare† (mesatarja):
  • 19 EHS - ACS-II Euro Heart Survey ka realizuar dy Vëzhgime për SKA (ACS) ACS-I në 2000-2001 25 shtete (103 qëndra) ACS-II në 2004 32 shtete (190 qëndra)
  • 20 Sindromi Koronar Akut në ACS I dhe IISindromi Koronar Akut në ACS I dhe II 42 51 7 47 48 5 0 10 20 30 40 50 60 SKANST SKAPST EKG e Papercaktuar % ACS I ACS II EHS - ACS-II
  • 21 ACS II - Diagnoza Fillestare dhe Përfundimtare EHS - ACS-II ST↑ 3004(47%) Pa-ST↑ 3063 (48%) IAM (75%) APP (25%) 95% 5% 55% 45%
  • 22 Vdekshmëria ACS-I / ACS-IIVdekshmëria ACS-I / ACS-II EHS - ACS-II 3.8 6.2 12.1 3.3 5.1 10.7 0 5 10 15 7 dite 30 dite 1vit % ACS-I ACS-II Pacientet Koha (muaj) Mbijetesa% Kurbat e mbijeteses te Kaplan-Meier ACS-IIACS-I
  • 23 Vdekshmëria spitalore e STEMI – IM NST nga 1994 - 2002 në Evropë Vdekshmeria spitalore e STEMI – IM NST Nga 1994- 2002
  • 24  SIZ është vrasësi më i madh iSIZ është vrasësi më i madh i Amerikanëve.Amerikanëve.  Çdo 26 sekonda një amerikan do tëÇdo 26 sekonda një amerikan do të vuajë nga një ngjarje koronarevuajë nga një ngjarje koronare..  ÇÇdo minut dikush do të vdesë ngado minut dikush do të vdesë nga njënjë ngjarje koronarengjarje koronare..  Rreth 40 % e personave që kalojnëRreth 40 % e personave që kalojnë një infarkt miokardi do të vdesin nganjë infarkt miokardi do të vdesin nga aiai brenda vititbrenda vitit Heart Disease and Stroke Statistics – 2006 UpdateHeart Disease and Stroke Statistics – 2006 Update Sindromi Koronar në SHBA
  • 25 Epidemiologjia eEpidemiologjia e SIZSIZ në SHBAnë SHBA 20062006 Semundjet KardiovaskulareSemundjet Kardiovaskulare TotaliTotali Prevalenca 2003Prevalenca 2003 71.3 Milion (M)(34.2%)71.3 Milion (M)(34.2%) Vdekshmeria 2003#Vdekshmeria 2003# 910.6 Mije910.6 Mije Semundja Ishemike e ZemresSemundja Ishemike e Zemres Prevalenca 2003 SIZPrevalenca 2003 SIZ 13.2 M (6.9%)13.2 M (6.9%) Prevalenca 2003 IMPrevalenca 2003 IM 7.2 M (3.5%)7.2 M (3.5%) Prevalenca 2003 APPrevalenca 2003 AP 6.5 M (3.8%)6.5 M (3.8%) Incidenca SIZ *Incidenca SIZ * 1.2 M1.2 Milionilion Incidenca IMIncidenca IM 865.0865.0 MijeMije Incidenca AP (APQ)Incidenca AP (APQ) 400.0400.0 MijeMije Vdekshmeria 2003 SIZ#Vdekshmeria 2003 SIZ# 479.3479.3 MijeMije Vdekshmeria 2003 IM#Vdekshmeria 2003 IM# 171.0171.0 MijeMije Heart Disease and Stroke Statistics – 2006 UpdateHeart Disease and Stroke Statistics – 2006 Update
  • 26 Perqindja e vdekjeve nga SAK ne grupin e SKV SHBA:2003 Source: CDC/NCHS. 6% 4% 13% 17% 6% 0,5% 0,4% 53% SAK Insulti IKK HTA Sem e arterieve SRZ Sem e lindura Te tjera
  • 27 Raporti vjetor i Infarktit te pare sipas Moshes, Gjinise, dhe Races. ARIC: 1987-2000 0 2 4 6 8 10 12 14 35-44 45-54 55-64 65-74 Mosha Per1,000Persona White Men Black Men White Women Black Women Source: NHLBI’s ARIC surveillance study, 1987-2000. Burra te Bardhe Burra te zinj Gra te bardha Gra te zeza
  • 28 Ngjarja e pare koronare:Ngjarja e pare koronare: Framingham StudyFramingham Study Ngjarja e specifikuar ne perqindjeNgjarja e specifikuar ne perqindje Infarkti IInfarkti I AnginaAngina Vdekja eVdekja e miokarditmiokardit PectorisPectoris papriturpapritur Mosha Burra Gra Burra Gra Burra GraMosha Burra Gra Burra Gra Burra Gra 35-64 43% 28%35-64 43% 28% 41% 59%41% 59% 9%9% 4%4% 65-8465-84 55% 44%55% 44% 28% 41%28% 41% 11% 7.4%11% 7.4% Framingham Study - 44 vjet ndjekje.Framingham Study - 44 vjet ndjekje. ____________________________________________________________ ________________________________________________________ ____________________________________________________________
  • 29 Rreziku i pasardhësve për SKV nëRreziku i pasardhësve për SKV në lidhje me prindërit me SKV:lidhje me prindërit me SKV: Framingham StudyFramingham Study 1 1.7 2.2 1 1.7 1.7 0 0.5 1 1.5 2 2.5 MESHKUJ FEMRA ASNJE AMTAR ATEROR Risk Ratio Adjusted for: age, total/HDL Chol. ratio, SBP, smoking, diabetes, BMI
  • 30 Aterotromboza shkurton ne menyre teAterotromboza shkurton ne menyre te rendesishme jetenrendesishme jeten Te dhena te analizuara nga Framingham Heart Study. Peeters A, et al. Eur Heart J. 2002;23:458-466. Aterotromboza ul shpresen per jeten rreth 8-12 vite tek pacientet me moshe mbi 60 vjec1 Mesatarja e Shpreses per jete qe mbete ne Moshen 60 vjec (Meshkuj) 0 4 8 12 16 20 I shendetshem Years Histori IAM -9.2 vite Histori per SKV -7.4 vite Histori insulti -12 vite
  • 31 CARDIOVASCULAR DISEASES IN ALBANIA PERHAPJA E SEMUNDJEVE NE SHQIPERI DHE BE NE 2004PERHAPJA E SEMUNDJEVE NE SHQIPERI DHE BE NE 2004 12818Demtimet ne total 838769Semundjet jongjitese ne total 9414Semundjet ngjitese ne total 554Crregullimet e organeve sensore 221Diabeti 322Demtimet e qellimshme 114Semundjet dhe kushtet perinatale 114Infeksionet respiratore 212Semundjet infektive dhe parazitare 372Semundjet respiratore jo infektive 9616Demtimet e paqellimshme 16179Kanceri/ Neoplazmat Malinje 212720Crregullimet neuropsikiatrike 221719 (7)Semundjet kardiovaskulare (SIZ) EU 10EU 15Shqiperia Shperdarja e semundjeve (%)Shkaku
  • 32 BE 15 17% 27% 17% 6% 7% 1% 1% 1% 2% 2% 5% 14% Semundjet Kardiovaskulare Crregullimet neuropsikike Kanceri/Neoplazmat malinje Demtimet e paqellimshme Semundjet respiratore joinfektive Semundjet infektive dhe parazitare Infeksionet respiratore Kushtet perinatale Demtimet e qellimshme Diabeti Crregullimet e organeve sensore Te tjera SHQIPERIA 19% 20% 9%16% 2% 2% 4% 4% 2% 1% 4% 17% Semundjet Kardiovaskulare Crregullimet neuropsikike Kanceri/Neoplazmat malinje Demtimet e paqellimshme Semundjet respiratore joinfektive Semundjet infektive dhe parazitare Infeksionet respiratore Kushtet perinatale Demtimet e qellimshme Diabeti Crregullimet e organeve sensore Te tjera CARDIOVASCULAR DISEASES IN ALBANIA PERHAPJA E SEMUNDJEVE NE SHQIPERI DHEPERHAPJA E SEMUNDJEVE NE SHQIPERI DHE BE-15 NE 2004BE-15 NE 2004
  • 33 Semundjet Kardiovaskulare ne Shqiperi 10 Shkaqet kryesore te vdekjeve ne10 Shkaqet kryesore te vdekjeve ne Shqiperi ne 2004Shqiperi ne 2004 ShkakuShkaku Vdekjet (%)Vdekjet (%) 1. Semundjet Cerebrovaskulare1. Semundjet Cerebrovaskulare 1919 2. Semundja Ishemike e zemres (SKV)2. Semundja Ishemike e zemres (SKV) 18 (52)18 (52) 3. Semundjet respiratore te poshtme3. Semundjet respiratore te poshtme 44 4. Kanceri Trakeal, bronkial, mushkerive4. Kanceri Trakeal, bronkial, mushkerive 44 5. Kanceri5. Kanceri ii stomakutstomakut 33 6. Kanceri6. Kanceri ii melcisemelcise 33 7. Semundjet dhe kushtet perinatale7. Semundjet dhe kushtet perinatale 22 8. Semundja hipertensive e zemres8. Semundja hipertensive e zemres 22 9. Nefriti dhe nefroza9. Nefriti dhe nefroza 22 10. Semundja pulmonare obstruktive kronike10. Semundja pulmonare obstruktive kronike 11
  • 34 Semundjet Kardiovaskulare ne Shqiperi 10 Shkaqet kryesore te vdekjeve ne10 Shkaqet kryesore te vdekjeve ne Shqiperi ne 2004Shqiperi ne 2004 52% 19% 4% 4% 3% 3% 2% 2% 1% 10% Semundjet KV Semundjet CV Semundjet respiratore te poshtme Kanceri trakeal, bronkial dhe i mushkerive Kanceri I stomakut Kanceri i melcise Kushtet perinatale Nefritis and nefrosis Semundja pulmonare obstruktive kronike Te tjera SHQIPERIA: 130 vdekje per 100 000. EU25 104 per 100000
  • 35 SKV gjatë vitit 2005 në QSUSKV gjatë vitit 2005 në QSU “Nënë Tereza”“Nënë Tereza” SIZ 30 %SIZ 30 % SKV ne QSUT 30% 12% 11% 8% 7% 7% 4% 7% 3% 11% SIZ Insulti HTA Crreg e ritmit dhe percimit SRZ Sem e arterieve Kardiomiopati e IK Varice Flebit Tromboflebit Te tjera
  • 36 Vdekshmëria KV gjatë 2005 nëVdekshmëria KV gjatë 2005 në QSU “Nënë Tereza”QSU “Nënë Tereza” Vdekshmeria e SKV ne QSUT 33% 23% 13% 5% 3% 6% 0% 17% SIZ Insulti Kardiomiopati e IK Crreg e ritmit dhe percimit SRZ Sem e arterieve HTA Te tjera
  • 37 Infarkti Akut i Miokardit deri në 2005 nëInfarkti Akut i Miokardit deri në 2005 në QSU “Nënë Tereza” TiranëQSU “Nënë Tereza” Tiranë 0 100 200 300 400 500 600 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 Vitet Noiinfarkteve IAM Ne vitin 2005 kane qene 2206 Semundje ishemike te zemres nder to 23,4 % (516) kane qene klasifikuar si IAM
  • 38 Angina Pectoris deri në 2005 nëAngina Pectoris deri në 2005 në QSU “Nënë Tereza” TiranëQSU “Nënë Tereza” Tiranë 0 200 400 600 800 1000 1200 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 Vitet Noiinfarkteve Angina Pectoris Në vitin 2005 kanë qënë 2206 Semundje ishemike të zemrës ndër to 43 % (944) kanë qënë klasifikuar si Angina Pectoris
  • 391. Adult Treatment Panel II. Circulation 1994; 89:1333–63. 2. Kannel ë et al. N Engl J Med 1992; 326: 381–6. Rreziku i rritur vs popullates ne pergjithesi (%) Ngjarja fillestare Infarkti I Miokardit Insulti Cerebral Infarkti I Miokardit Insulti Cerebral SAP 5–7 x risk me i madh1 (perfshire vdekjet) 3–4 x risk me i madh2 (perfshite TIA) 2–3 x risk me i madh2 (perfshire anginen e vdekjen e papritur) 9 x risk me i madh3 4 x risk me i madh4 (perfshire vetem IM fatal dhe vdekjet SAK) 2–3 x risk me i madh3 (perfshire TIA) Rreziku për një Ngjarje të DytëRreziku për një Ngjarje të Dytë VaskulareVaskulare
  • 40 Identifikimi I personave në rrezik përIdentifikimi I personave në rrezik për AterotrombozëAterotrombozë1,21,2 1. Yusuf S et al. Circulation 2001; 104: 2746–53. 2. Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 1–6. Stili I jetes • Duhani • Dieta • Inaktiviteti Faktoret gjenetike • Te dhenat gjenetike • Gjinia • Mosha Crregullimet e pergjitheshme • Obeziteti • Diabeti Gjendjet sitemike • Hisori per ngjarje vaskulare • HTA • Hiperlipidemia • Gjendjet hiperkoagulative • Homocistinemia Faktoret lokale: • Faktoret protrombike te rritur: fibrinogjen, CRP, PAI-1 • Parametrat e fluksit vazal, diametrat vazale, struktura e murit arterial Manifestimet Aterotrombitike (IM, Insult, vdekja vaskulare)
  • 41 Ngjarjet aterotrombotike /100 Paciente ne vit Ngjarjet aterotrombotike sipas faktoreveNgjarjet aterotrombotike sipas faktoreve te riskutte riskut11 1. Caro J. Eur Heart J 2001; 22(abstr suppl): 522. RaportiIngjarjevevjetore(%) Numri I faktoreve te riskut % 21.8% 5.5% % % % % % 0–1 2–3 4–5 6–7 8 ose me teper 0 5 10 15 20 25
  • 42 Popullatat me moshë mbi 65 vjeç në Europë Popullatat me moshë mbi 65 vjeç Përqindja e popullatës mbi 65 vjeç Cardiovascular Diseases in Europe. Euro Heart Survey 2006 Updated Heart Disease and Stroke Statistics – 2006Heart Disease and Stroke Statistics – 2006 UpdateUpdate Në Evropë 13,7% e popullatës është 65 vjeçare dhe është dyfishi i nivelit botëror. Perqindja e personave mbi 65 vjeç në Evropë do të rritet me 30% në 2050. Në SHBA do të rritet me 20 % në 2035. Perqindja
  • 43 Jetëgjatesia në Evropë 2004Jetëgjatesia në Evropë 2004 Cardiovascular Diseases in Europe. Euro Heart Survey 2006 Updated Jetegjatesia Piramida e moshave në 2004 Piramida e moshave në 2050 Mosha mesatare është 75.11 vjeç. Nga 1980 ne 2004 Jetegjatesia eshte rritur nga 71.3 ne 75.11 vjeç
  • 44 Stili i jetes tek personat me SAK 59 50 33 22 67 55 25 21 0 10 20 30 40 50 60 70 80 90 100 Kolesteroli > 200 mg/dl Tensioni arterial > 140/90mmHg IMT > 30kg/m2 duhanpirja % 1995 - 1996 2000 - 2001 Cardiovascular Diseases in Europe. Euro Heart Survey 2006 Updated EHS – Vëzhgimi EUROASPIRE I & II
  • 45 EHS: Duhanpirësit në Europe në 2004EHS: Duhanpirësit në Europe në 2004 Cardiovascular Diseases in Europe. Euro HeartCardiovascular Diseases in Europe. Euro Heart Survey 2006.Survey 2006. WHO EUROPE 10 health questionsWHO EUROPE 10 health questions about the new EU neighborsabout the new EU neighbors.. AHA, Heart DiseaseAHA, Heart Disease and Stroke Statistics – 2006 Update.and Stroke Statistics – 2006 Update. Duhanepirësit mbi 15 vjeç Perqindja < 20 20 deri 25 25 deri 30 30 deri 35 35 deri 40 Pa te dhena Rreth 20%- 29% në Europë dhe SHBA pijnë duhan, në Shqipëri edhe më shumë rreth 39%. ( 60% për meshkujt dhe 18% për femrat). Në Shqipëri duhanpirja shkakton 22% të sëmundshmërisë. Në botë në 1990 shkaktoi 6% të vdekshmërisë dhe në 2020 do të shkaktojë 12% James W. Levenson, MD et al.James W. Levenson, MD et al.Reducing the Global Burden of Cardiovascular Disease: The Role of Risk FactorsReducing the Global Burden of Cardiovascular Disease: The Role of Risk Factors Preventive CardiologyPreventive Cardiology 01/21/200301/21/2003
  • 46 Cardiovascular Diseases in Europe. Euro Heart Survey 2006 Updated,Cardiovascular Diseases in Europe. Euro Heart Survey 2006 Updated, WHO EUROPE 10 healthWHO EUROPE 10 health questions about the new EU neighborsquestions about the new EU neighbors AHA, Heart Disease and Stroke Statistics – 2006 UpdateAHA, Heart Disease and Stroke Statistics – 2006 Update Obeziteti në Europe në 2004Obeziteti në Europe në 2004 BMI ≥ 30 kg/m2, Burra BMI ≥ 30 kg/m2, Gra Perqimdja < 10 10 deri 15 15 deri20 20 deri25 > 25 Pa te dhena Perqimdja < 10 10 deri 15 15 deri20 20 deri25 > 25 Pa te dhena Rreth 30 % e Evropianëve e kane Indeksin e masës trupore mbi 30kg/m2, dhe 25% e Amerikanëve. Në Shqipëri 24% e burrave dhe 20% e grave janë obezë. Obeziteti shkakton rreth 10 % të sëmundshërisë, dhe inaktiviteti fizik 5,3 %
  • 47 Pacientët me Diabet në Europe nëPacientët me Diabet në Europe në 20042004 Cardiovascular Diseases in Europe. Euro Heart Survey 2006Cardiovascular Diseases in Europe. Euro Heart Survey 2006 AHA,AHA, Heart Disease and Stroke Statistics – 2006 UpdateHeart Disease and Stroke Statistics – 2006 Update Prevalenca e glukozes jo normale ne pacientet me sindrom koronar akut Diabeti i njohur 33% Diabeti i ri 13% Tolerance e demtuar ndaj glukozes 23% Normal 28% Diabeti, Mosha 20- 79 Glicemi esell e demtuar 3% Rreth 7% kanë Diabet ne Europë dhe 7,5 % në Amerikë, rreth 4 % ne mbarë botën. Se paku 65% e njerezve me DM vdesin nga ndonje semundje e zemres ose e vazave Prevalenca e diabetit ne mbare boten u vleresua 2.8% ne 2000 dhe projektohet ne 4.4% ne 2030. . James W. Levenson, MD et al.James W. Levenson, MD et al.Reducing the Global Burden of Cardiovascular Disease: The Role of Risk FactorsReducing the Global Burden of Cardiovascular Disease: The Role of Risk Factors Preventive CardiologyPreventive Cardiology 01/21/200301/21/2003
  • 48 Vdekjet e parandalueshmeVdekjet e parandalueshme Me mijera vdekje mund te shmangen çdo vit në SHBA nëse pacientëve i jepet ndihma e duhur National Committee for Quality Assurance. Washington, DC 2003. Ndalimi i duhanit Kontrolli i Kolesterolit Trajtimi I Diabetit Kontrolli I hipertensionit arterial 2700 6500 13,600 28,300
  • 49 FIZIOPATOLOGJIAFIZIOPATOLOGJIA Pas 1980 u konstatua se tromboza ishte shkaku i SKA. Teknikat imazherike in vivo dhe sukseset e terapise anti- trombotike e fibrinolitike vendosen ne praktike rolin e trombozes ne patogjenezen e SKA. SKA eshte reduktim fillestar i menjehershem ose pak me gradual i furnizimit me O2 te miokardit si pasoje e carjes, erozionit, ose hemorragjise se pllakes aterosklerotike te paqen- drueshme e shoqeruar me inflamacion, tromboze, vazokonstriksion e mikroemboli distale Fisurat ne kapsulen fibroze Fisurat ne kapsulen fibroze
  • 50 Percaktimi i Sindromi Koronar Akut APP IM pa vale Q IM-NST Ruptura/Fisura/Erozioni i pllakes Formimi i trombit Sindromi Akut Koronar Pa Ngritje te ST (SKA-PNST) Sindromi Akut Koronar me Ngritje te ST (SKA-NST) Terminologjia e vjeter: Terminologjia e re:
  • 51 Karakteristikat e pllakës sëKarakteristikat e pllakës së qëndrueshme dhe të paqëndrueshmeqëndrueshme dhe të paqëndrueshme Kapsule e holle fibroze Qelizat inflamatore Pak QML Endotel i erozionuar Makrofaget e aktivizuar Kapsule e trashe fibroze Mungese e Qelizave inflamatore Qelizat shkumoze Endotel i paprekur Shume QML Libby P. Circulation. 1995;91:2844-2850.. Available at:www..theheart.org. Paqendrueshme Qendrueshme
  • 52 Faktorët e rrezikut për Rupturën eFaktorët e rrezikut për Rupturën e pllakëspllakës Fibrinoliza e demtuar Fibrinogjeni Diabeti Mellitus Kolesteroli DuhanpirjaDemtimi i Kapsules Inflamacioni i kapsules Faktoret sistemikeFaktoret Lokale Homocisteina Ruptura e pllakes Fuster V, et al. N Engl J Med. 1992;326:310-318. Falk E, et al. Circulation. 1995:92:657-671. Hollimi/ Konsistenca i kapsules Berdhama lipidike
  • 53 Format e dëmtimit të pllakësFormat e dëmtimit të pllakës aterosklerotikeaterosklerotike Nyja Kalcike Hemorragjia brenda pllakes Mikrovazat Ruptura e Kapsules Fibroze (2/3 SKA) Erozioni siperfaqesor Erozioni I Nodusit Kalcik Hemorragjia brenda pllakes
  • 54 PPëërcaktuesit e trombozrcaktuesit e trombozëës ns nëë pllakpllakëën aterosklerotiken aterosklerotike Ne Fazen FluideNe Fazen Fluide ndryshojnendryshojne mmediatoretediatoret antifibrinolitike eantifibrinolitike e protrombotike (rritetprotrombotike (rritet PAI -1 e TNF )PAI -1 e TNF ) Ne fazen solideNe fazen solide  DisfunksioniDisfunksioni endotelial,endotelial,  AktivizimiAktivizimi i morkroi morkro-- fagevefageve  Proliferimi e apoptozaProliferimi e apoptoza e QMLe QML Percaktuesit e Fazes Fluide Percaktuesit e Fazes Solide
  • 55 Ruptura e Pllakës çon nëRuptura e Pllakës çon në Formimin e AterotrombozësFormimin e Aterotrombozës Adapted from: Falk E et al. Circulation 1995; 92: 657–71. Makrofaget Faktori indor Fibrina Ttombocitet e agreguara Rrjedha e gjakut
  • 5656 1. Adezioni trombocitar 2. Aktivizimi trombocitar Trombocit GP Ib Ruptura e pllakes Trombocitet e akt. GP IIb/IIIa 3. Agregimi trombocitar Cannon and Braunëald, Heart Disease. 2001. TxA2 Fibrinogjeni Roli i trombociteve në aterotrombozëRoli i trombociteve në aterotrombozë
  • 57 Adezioni MediatorëtMediatorët kkyç në adezionin,yç në adezionin, aktivizimin e agregimin trombocitaraktivizimin e agregimin trombocitar 1. Ferguson JJ. The Physiology of Normal Platelet Function. In: Ferguson JJ, Chronos N, Harrington RA (Eds). Antiplatelet Therapy in Clinical Practice. London: Martin Dunitz; 2000: pp.15–35. DEMTIMI • FvW • Trombina • Kolagjeni • Fibronektina Stresi muror FvW Receptori - ADP TROMBI Aktivizimi Agregimi • Ndryshimet e membranes trombocitare • Sekretimi granular T, makrofaget, QML • Receptoret GPIIb/IIIa • Kolagjen, tromboksani, ADP, trombina • Efekti feed back • ndermjetesimiGPIIb/IIIa • Fibrinogjeni • FvW Aktivizimi trombocitar dhe faktoret indore aktivizojne kaskaden e koagulimit
  • 58 Ruptura e pllakes Aktivizimi dhe agregimi trombocitar Trombi jo oklusiv Sindromat akute: • koronare • cerebrovaskulare • periferikeTrombi okluziv Shërimi dhe shkrirja Rritja e plakes, rimodelimi vaskular Zhvillimi iZhvillimi i aaterotrombozës –terotrombozës – njënjë pproçesroçes ii ggjeneralizuar dhejeneralizuar dhe pprogresivrogresiv Adapted from: Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 1–6.
  • 59 Rimodelimi KoronarRimodelimi Koronar VazeVaze normalenormale SAKSAK minimalminimal PerparimiPerparimi Shperndarja kompensatoreShperndarja kompensatore mban lumeninmban lumenin konstant Zenia e lumenit:Zenia e lumenit: NgushtimiNgushtimi SAKSAK i rendei rende SAKSAK i moderuari moderuar Glagov et al,Glagov et al, N Engl J MedN Engl J Med, 1987., 1987.
  • 60 Infarktet më të shumtë të miokarditInfarktet më të shumtë të miokardit Shkaktohen nga Stenoza jo sinjifikanteShkaktohen nga Stenoza jo sinjifikante Te dhena te marra nga 4 studime: Ambrose et al, 1988; Little et al, 1988; Nobuyoshi et al, 1991; dheTe dhena te marra nga 4 studime: Ambrose et al, 1988; Little et al, 1988; Nobuyoshi et al, 1991; dhe Giroud et al, 1992.Giroud et al, 1992. (Adapted from Falk et al.)(Adapted from Falk et al.) Falk E et al, Circulation, 1995. Rendesa e stenozave koronare para IM 68% 18% 14% 50% - 70% Stenoze >70% Stenoze <50% Stenoze
  • 61 Aterotromboza dhe MikroqarkullimiAterotromboza dhe Mikroqarkullimi Adapted from: Topol EJ, Yadav JS. Circulation 2000; 101: 570–80, and Falk E et al. Circulation 1995; 92: 657–71. Ruptura e pllakes Obstruksioni mikrovaskular Embolia Mikroembolat te pasura me faktor indor qe ndodhin kur nje pllake eshte e rupturuar, japin trombozen distale ne mikroqarkullim. Keto embolizime distale shpjegojne fenomenin ”no- reflow”, kjo nuk lejon reperfuzionin efektiv te mikroqarkullimit distal
  • 62 SKA: Maja e “Ajsbergut” Aterotrombotik Goldstein JA. J Am Coll Cardiol. 2002;39:1464-1467. Prania e pllakave te shumefishta koronare Inflamacioni koronar Trombocitet Hiperreaktive persistente Klinike Subklinike Ruptura Akute e Pllakes SKA (APP/ IM PNST/ IM NST) Lezione te tjera aterosklerotike jane te perhapura ne sistemin arterial koronar njekohesisht me lezionin pergjegjes per SKA. Keto lezione jane me pak severe, me pak stenozuese, me pak te kalcifikuara. Pra SKA duket se eshte i shoqeruar me nje “destabilizim” pankoronar
  • 63 Koncepti i Pllakave te shumefishtaKoncepti i Pllakave te shumefishta aterosklerotike (1)aterosklerotike (1) Koronarografi IVUS
  • 64 Muri i RCAMuri i LAD Eksentrike (“pasur me lipide”) Koncentrike (“fibrotike”) Ektazike (“rimodeluar”) Koncepti i Pllakave te shumefishtaKoncepti i Pllakave te shumefishta aterosklerotikeaterosklerotike (RM) (2) MR, magnetic resonance; LAD, left anterior descending; RCA, right coronary artery. Fayad ZA, et al. Circulation. 2000;102:506-510. (with permission from Lippincott Williams & Wilkins, www.lww.com) Muri I LAD
  • 65 Pllakat e shumëfishta KoronarePllakat e shumëfishta Koronare komplekse në pacientët me IM akut (3)komplekse në pacientët me IM akut (3) Goldstein JA, et al. N Eng J Med. 2000;343:915-922. (Copyright © 2000 Massachusetts Medical Society. All rights reserved) Lezioni kryesorLezioni kryesor Pllaka të shumëfishtaPllaka të shumëfishta koronarekoronare Pllaka të shumëfishtaPllaka të shumëfishta koronarekoronare Pllaka të shumëfishtaPllaka të shumëfishta koronarekoronare Pllaka të shumëfishtaPllaka të shumëfishta koronarekoronare
  • 66Rioufol G, et al. Circulation 2002;106:804-808. Shpeshtësia e Rupturave te Pllakave “Aktive” të shumëfishta perveç lezionit kryesor per IM. Megjithese nje lezion I vetem eshte klinkisht aktiv ne pacientet me SKA, sindromi duket se shoqerohet me nje destabilizim pankoronar Paciente(%) 80% e pacienteve kane ≥ 2 Pllaka 0 5 10 15 20 25 30 0 1 2 3 4 5 N=24 Shpeshtësia e Pllakave “Aktive” të shumëfishta në Pacientët me SKA (4)
  • 67 Yeghiazarians Y, Braunstein JB, Askari A, et al. Unstable angina pectoris. N Engl J Med. 2000;342:101-114. Pllaka e paqendrueshme •Qender te madhe eksentrike te mbushur me lipide •Infiltrimi i qelizave shkumoze ne qendren lipidike duke sekretuar faktorin indor •Kapsule fibroze te holle •Mjedis lokal inflamator, neutrofile, qeliza LT, makrofage, qeliza te muskulatures se lemuar, dhe citokina qe nxisin çarjen e kapsules nepermjet sekretimit te metaloproteinazave. Linfocitet T Trombocitet Linfocitet T Trombocitet Kapsula fibroze Berthama lipidike Qelizat shkumoze Qel. Musk. lemuar Formimi i trombit Trombogjeniciteti sistemik. •Aktivizimi, Adezioni, dhe Agregimi trombocitar. •Aktivizimi i shtegut te Koagulimit dhe formimit te trombines •Kthimi i fibrinogjenit ne fibrine me lidhje kryqe Ruptura e pllakes Faktoret shperthyes: ushtrimi fizik, stresi mekanik pasoje e rritjes se kontraktilitetit, frekuences kardiake, tensionit arterial, dhe mundesisht, vazokonstriksioni Qelizat shkumoze Qel. Musk. lemuar Fibrina Okluzioni i plote koronar Liza spontane, riparimi, dhe rimodelimi mural Okluzioni Jo i plote koronar Përmbledhje Infarkt Akut i Miokardit Zgjidhja e perkoheshme e gjendjes Lezione koronare me rrezik te larte Angina e paqendrueshme IM pa vale Q
  • 68 Ju faleminderitJu faleminderit Tiranë më 16.12.2006