1) Sudden cardiac death is often the first clinical manifestation of coronary artery disease and can result from vulnerable plaque rupture leading to coronary occlusion or electrical abnormalities.
2) Autonomic factors influence the clinical outcome of coronary occlusion, with increased heart rate variability associated with vagal activation reducing the risk of ventricular arrhythmias, while decreased heart rate variability due to vagal withdrawal increases the risk.
3) The site of coronary occlusion also influences outcomes, with left anterior descending artery occlusion more often associated with ventricular arrhythmias compared to other sites of occlusion. Genetic factors may also influence individual responses.
ARVD is one of important coardiomyopathy in our clinical practice,early diagnosis, risk stratification and early diagnosis of CHF, management of VT will make big difference in patient life
ARVD is one of important coardiomyopathy in our clinical practice,early diagnosis, risk stratification and early diagnosis of CHF, management of VT will make big difference in patient life
Reverse Takotsubo Cardiomyopathy Following General AnaesthesiaPremier Publishers
Reverse takotsubo cardiomyopathy(r-TTC) is a rare condition in which regional wall motion abnormalities affect the basal segments of left ventricle in absence of significant coronary artery disease. The Diagnosis is established by characteristic echocardiographic findings, clinical manifestations, and laboratory features. In this report we demonstrate a case of general anaesthesia induced cardiomyopathy in 21 years old female.
Papillary fibroelastoma, a primary cardiac tumour commonly found on the cardiac valves is less frequently found on the non-valvular myocardium. Most non-valvular papillary fibroelastomas are confined to the left ventricle and the atrial origin of this tumour is rare. We present a case of papillary fibroelastoma originating from the left atrial ridge or the Coumadin ridge (the confluence of the long axis of the left upper pulmonary vein with the roof of the left atrial appendage). There are a few sporadic reports of the origin of papillary fibroelastomas from the left atrial ridge and the majority of these have presented with cerebral embolism. These uncommon tumours have a predilection to cause embolic phenomenon, especially those arising from the left atrial ridge.
Review of a rare but important cardiac dysplasia causing high mortality and morbidity in mostly young patients.
In this presentation, the epidemiology, pathophysiology, diagnosis and treatment of said disease is examines.
Reverse Takotsubo Cardiomyopathy Following General AnaesthesiaPremier Publishers
Reverse takotsubo cardiomyopathy(r-TTC) is a rare condition in which regional wall motion abnormalities affect the basal segments of left ventricle in absence of significant coronary artery disease. The Diagnosis is established by characteristic echocardiographic findings, clinical manifestations, and laboratory features. In this report we demonstrate a case of general anaesthesia induced cardiomyopathy in 21 years old female.
Papillary fibroelastoma, a primary cardiac tumour commonly found on the cardiac valves is less frequently found on the non-valvular myocardium. Most non-valvular papillary fibroelastomas are confined to the left ventricle and the atrial origin of this tumour is rare. We present a case of papillary fibroelastoma originating from the left atrial ridge or the Coumadin ridge (the confluence of the long axis of the left upper pulmonary vein with the roof of the left atrial appendage). There are a few sporadic reports of the origin of papillary fibroelastomas from the left atrial ridge and the majority of these have presented with cerebral embolism. These uncommon tumours have a predilection to cause embolic phenomenon, especially those arising from the left atrial ridge.
Review of a rare but important cardiac dysplasia causing high mortality and morbidity in mostly young patients.
In this presentation, the epidemiology, pathophysiology, diagnosis and treatment of said disease is examines.
R. Loch Macdonald, M.D., Ph.D.
Community Neurosciences Institute
Fresno, California, USA
Angiographic vasospasm and more accurately, delayed cerebral ischemia, continue to contribute to morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). It is known that angiographic vasospasm is common after SAH, occurring in two-thirds of patients. Cerebral infarctions that developed days after the SAH have been attributed to angiographic vasospasm, occuring in about a third of patients, although this has always been controversial. Angiographic vasospasm theoretically can only damage the brain by restricting blood flow but there is no easy, accurate, widely available method to measure cerebral blood flow and this is not the measurement we need. Blood flow depends on metabolic demand so what we need to know to determine if angiographic vasospasm is causing ischemia is oxygen extraction fraction in the brain tissue supplied the the spastic artery. Without this measurement, the attribution of ischemia to vasospasm is subjective. Since angiographic vasospasm is essentially the only detectable delayed phenomenon after SAH, we focus on it and apply tremendous resources to preventing or reversing the vasospasm. Undoubtedly angiographic vasospasm can cause cerebral infarctions, but it has to be severe and flow limiting. But SAH is a complex disease. There are many other causes for cerebral infarctions after SAH, the most common being due to the aneurysm repair procedure. And a given degree of vasospasm may cause infarction in a volume-depleted patient with poor collateral blood supply but not in a patient without these things. There also are hypodense brain lesions after SAH that are due to intracerebral hemorrhages. There can be hypodensities in the brain directly under usually thick SAH where the brain dies. This observation in particular supports a role for cortical spreading depolarizations/ischemia as a cause of infarction after SAH. Other macromolecular processes that are hypothesized to cause brain damage after SAH include microthromboembolism, changes in the microcirculation, delayed brain cell apoptosis and capillary transit time heterogeneity. Determining the importance of these things is hindered by the lack of an easy way to detect them in patients. It is also known that poor grade patients, who presumably have more early brain injury and ischemia than good grade patients, are more prone to delayed cerebral ischemia, suggesting increased sensitivity to secondary insults of the already injured brain. We also assume delayed neurological deterioration when attributed to vasospasm or delayed cerebral ischemia, is purely due to ischemia. While knowledge about what happens pathophysiologically after SAH is increasing, management of delayed cerebral ischemia still focuses on detecting angiographic vasospasm and then augmenting the blood pressure to improve cerebral blood flow or dilating the spastic arteries with balloons or drugs.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
3. Occlusive Plaque rupture:
Sudden death, usually occurring within
minutes of the onset of chest pain, is the
first clinical manifestation of CAD in 20-
25% of patients
40% of deaths occur within 1h after
AMI
Kannel et al, Circulation 1975;51:606
4. Sudden Cardiac Death
General Adult (”Healthy”) Population
♦ Pathophysiology:
1) Coronary plaque rupture coronary occlusion
SCD
2) Electrical or mechanical abnormality
– WPW-syndrome
– Long QT-syndrome
– idiopatic VF, Brugada syndrome...
– HOCM, ARVD, myocarditis...
5. ”Why do some people die
when a coronary artery
suddenly occludes
……and others develop only a
myocardial infarction or UAP?”
7. Control
Single Cardiac Vagal Fiber Activity LAD
Occlusion and Risk of Sudden Death (Cats)
1
2
3
4 VF-
VF+
Occlusion
Imp/s P<0.01
Cerati et al 1991
8. Prevention of VF after Left Stellate
Ganglionectomy in Dogs
0
20
40
60
80
100 LSG
Control
20 min coronary occlusion
Puddu et al 1988
P=0.001
Survival
%
9. PTCA-model to Simulate Coronary
Occlusion
2 min coronary occlusion
≈ 500 pts
♦ Beat-to-beat RRi and BP
♦ Ventricular arrhythmias
♦ Repolarisation changes
♦ MSNA
↔Interventions: ß-blockade
α-stimulation
10. Continuous ECG, Heart Rate and BP Recordings
RR interval
(ms)
Blood
pressure
(mmHg)
RR interval
(ms)
Blood
pressure
(mmHg)
11. HRV and Sudden Cardiac Death
Malignant ventricular arrhythmias caused
by abrupt coronary occlusion
are a major cause of sudden death
20. HRV Responses and Site of Coronary Occlusion
66%
23%
11%
26%
11%
63%
26%
21%
53%
LAD LCX RCA
Airaksinen et al Am J Cardiol 1993
Vagus Vagus
21. Gender Difference in Autonomic and
Hemodynamic Reactions
Reactions in women versus men
Adjusted OR (95% CI)
Bradycardia 3.8 (1.6-8.9)
RMSD 1.8 (0.8-4.1)
Hypotension 2.6 (1.1-6.1)
B-J Reaction 25.6 (2.6-254)
VEBs 0.4 (0.2-1.3)
Airaksinen et al JACC 1998
22. Is a Mild Stenosis More Hazardous??
♦SCD is the 1st symptom of CAD in 20-25%
♦Experimental models:
Coronary occlusion VF
Tight stenosis:
♦Occlusion often asymptomatic
♦Restenosis: SCD infrequent
♦Reocclusion: 50% asymptomatic
23. Stenosis Severity and the Occurrence of
Ventricular Ectopic Activity During Acute
Coronary Occlusion
0
10
20
30
VPBs(%)
*
< 75 75-89 90-99
Stenosis severity (%)
Airaksinen et al Am J Cardiol 1995b
P<0.01
P<0.01
24. Effect of Preocclusion Stenosis Severity on
Heart Rate Reactions to Coronary
Occlusion
26%
42%
32%
83%
17%
≤ 85% > 85%
Severity of stenosis
Airaksinen et el Am J Cardiol 1994
Vagus
Vagus
25. Adaptation Phenomena
• Psychological adaptation helpful in experimental
models (Parker et al 1987)
• Missile War or earthquake: sharp rise in incidence
of SCD during 1st attack, but not later (Meisel et al 1991)
• Short coronary occlusions lead to preconditioning
and adaptation in experimental models
27. Genetic Factors?
• No direct evidence, but...
• Clinical and angiographic factors poor
predictors
• Genetic background in wide interindividual
variation in autonomic function (Singh et al Circulation
1999)
• Parental history of SCD (Jouven et al Circulation 1999)
28. How to Modify the Risk?
• Plaque
modification
• Beta blockade
• Exercise ( Billman et al
Circulation 1984,Burke et al JAMA
1999)
29. Conclusions
Plaque rupture is the major cause of sudden death
at population level
Autonomic mechanisms modify significantly
clinical outcome
Clinical outcome is largely unpredictable
Plaque modification is the best way to modify the
outcome
30. Occluded coronary artery
LAD (58%)
LCX (21%)
RCA (21%)
LAD (79%)
LCX (5%)
RCA (5%)
LAD (93%)
LCX (7%)
No VA
(N=219
Solitary VA
(N=19)
Complex VA
(N=14)
34. Can we modify HRV and is it
useful ?
Pikkujämsä et al
35. Low HRV
A marker of arrhythmic death
• Observational studies: (Farrell et al 1991, Bigger et al 1992,1993,
Algra et al 1993, Hartikainen et al 1996, Copie et al 1996, Bigger et al 1996)
Problem: Definition of sudden death
• Case control studies (Huikuri et al 1995, Perkiömäki et al 1997)
Problem: Matching, HRV measurement after the end
point
• HRV is altered before the onset of VF / VT in pts
with a history of MI (Valkama et al 1995, Huikuri et al 1996,
Shusterman et al 1998, Vybiral et al 1993)
36. HRV and sudden cardiac death
• Is the positive predictive accuracy enough for
clinical decisions ?
- SDNN ( Nordic ICD Pilot Study): 1/33 appropriate
shocks / 2 yr
• Depressed HRV identifies post-MI pts who might benefit
from AMIO (EMIAT substudy, Malik et al, JACC 2000)
- new nonlinear indices better (?)