The document discusses the relationship between air pollution and cardiovascular disease. It notes that levels of air pollutants have increased since the Industrial Revolution and are associated with hundreds of thousands of deaths per year from cardiovascular causes. Air pollution consists of particulate matter and gases that can be inhaled and cause oxidative stress, pulmonary and systemic inflammation, and autonomic nervous system imbalances leading to increased risk of cardiac arrhythmias, myocardial infarction, heart failure and mortality. Both outdoor and indoor air pollution exposure are linked to elevated cardiovascular disease risks.
Presentation by D Prabhakaran DM during the panel on 'Health Effects of Exposure to Air Pollution, as part of the CPR Initiative on Climate, Energy and Environment Clearing the Air Seminar Series. This event was organised in partnership with the Public Health Foundation of India (PHFI)
Various coronary physiological measurements can be made in the cardiac catheterization laboratory using sensor-tipped guidewires; they include the measurement of poststenotic absolute coronary flow reserve, the relative coronary flow reserve, and the pressure-derived fractional flow reserve of the myocardium. Ambiguity regarding abnormal microcirculation has been reduced or eliminated with measurements of relative coronary flow reserve and fractional flow reserve. The role of microvascular flow impairment can be separately determined with coronary flow velocity reserve measurements. In addition to lesion assessment before and after intervention, emerging applications of coronary physiology include the determination of physiological responses to new pharmacological agents, such as glycoprotein IIb/IIIa blockers, in patients with acute myocardial infarction. Measurements of coronary physiology in the catheterization laboratory provide objective data that complement angiography for clinical decision-making
Presentation by D Prabhakaran DM during the panel on 'Health Effects of Exposure to Air Pollution, as part of the CPR Initiative on Climate, Energy and Environment Clearing the Air Seminar Series. This event was organised in partnership with the Public Health Foundation of India (PHFI)
Various coronary physiological measurements can be made in the cardiac catheterization laboratory using sensor-tipped guidewires; they include the measurement of poststenotic absolute coronary flow reserve, the relative coronary flow reserve, and the pressure-derived fractional flow reserve of the myocardium. Ambiguity regarding abnormal microcirculation has been reduced or eliminated with measurements of relative coronary flow reserve and fractional flow reserve. The role of microvascular flow impairment can be separately determined with coronary flow velocity reserve measurements. In addition to lesion assessment before and after intervention, emerging applications of coronary physiology include the determination of physiological responses to new pharmacological agents, such as glycoprotein IIb/IIIa blockers, in patients with acute myocardial infarction. Measurements of coronary physiology in the catheterization laboratory provide objective data that complement angiography for clinical decision-making
Today, in addition to measurement of left ventricular ejection fraction, the simple 12-lead surface ECG remains the only evidence-based means of identifying patients who may obtain the substantial benefits of CRT
ECHOCARDIOGRAPHIC EVALUATION OF MITRAL VALVE DISEASEPraveen Nagula
MITRAL VALVE ANATOMY , M MODE FINDINGS IN MITRAL STENOSIS,EVALUATION OF THE SEVERITY OF LESION,CALCIFIC MS,CCMA,CONGENITAL LESIONS,GUIDELINES ALL IN DETAIL....
Coronary artery disease (CAD) also known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease, or ischemic heart disease (IHD), is the most common type of heart disease and cause of heart attacks. The disease is caused by plaque building up along the inner walls of the arteries of the heart, which narrows the lumen of arteries and reduces blood flow to the heart.
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.
The diagnosis of biatrial enlargement requires criteria for LAE and RAE to be met in either lead II, lead V1 or a combination of leads.
Today, in addition to measurement of left ventricular ejection fraction, the simple 12-lead surface ECG remains the only evidence-based means of identifying patients who may obtain the substantial benefits of CRT
ECHOCARDIOGRAPHIC EVALUATION OF MITRAL VALVE DISEASEPraveen Nagula
MITRAL VALVE ANATOMY , M MODE FINDINGS IN MITRAL STENOSIS,EVALUATION OF THE SEVERITY OF LESION,CALCIFIC MS,CCMA,CONGENITAL LESIONS,GUIDELINES ALL IN DETAIL....
Coronary artery disease (CAD) also known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease, or ischemic heart disease (IHD), is the most common type of heart disease and cause of heart attacks. The disease is caused by plaque building up along the inner walls of the arteries of the heart, which narrows the lumen of arteries and reduces blood flow to the heart.
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.
The diagnosis of biatrial enlargement requires criteria for LAE and RAE to be met in either lead II, lead V1 or a combination of leads.
Based on money and Materials Our modern life became a big illusion. The Real life and happiness needs 1- Security 2- Health 3- Life essentials (food – shelter etc). The Real life and happiness lie behind a natural life in a clean environment. We are sinking in different types of pollution. The consequences of pollution include: 1- Climate change the Heat melts ice, worsens weather and expands oceans. 2- Human health effects a- Climate changes b- Pollutants. 3- Plants and animals Natural habitats become hostile. Pollution is a Global Problem with no but a Single must be a Global Solution that is Go Green, Reduce CO2 and Stop Pollution.
Smoking represents the most readily preventable risk factor for morbidity and mortality.
Smoking related disease will kill one in 10 adults globally.
There are more than 6 million smoker in KSA that represent about 30% from population in 2004.
Smoking and Cardiovascular Disease:
coronary artery disease
cardiac arrhythmias.
Atherosclerosis
Cigarette smoking increases blood cholesterol levels, causing a buildup of arterial plaque that narrows the blood vessels over time.
Blood Clots
Low Blood Oxygen
stroke
Air pollution is the contamination of air due to the presence of substances in the atmosphere that are harmful to the health of humans and other living being ,or cause damage to the climate or to materials.
Air pollution is a familiar environmental health hazard. We know what we’re looking at
when brown haze settles over a city, exhaust billows across a busy highway, or a plume
rises from a smokestack. Some air pollution is not seen, but its pungent smell alerts you.
It is a major threat to global health and prosperity. Air pollution, in all forms, is responsible
for more than 6.5 million deaths each year globally, a number that has increased over the
past two decades.
Air pollution is a mix of hazardous substances from both human-made and natural sources.
Vehicle emissions, fuel oils and natural gas to heat homes, by-products of manufacturing
and power generation, particularly coal-fueled power plants, and fumes from chemical
production are the primary sources of human-made air pollution.
Nature releases hazardous substances into the air, such as smoke from wildfires, which are
often caused by people; ash and gases from volcanic eruptions; and gases, like methane,
which are emitted from decomposing organic matter in soils.
Effect of Cigarette Smoking on cardiovascular and Respiratory Systems
Discuss the epidemiology of smoking in KSA
List the ill-health effects of smoking on CVS and respiratory system and describe their patho-physiology.
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4. Introduction
• Levels of environmental pollutants have increased since the Industrial Revolution.
• Air pollutants emitted by industrial, traffic, household, and agricultural sources
• 200,000 deaths in the United States, 1.6 million death in China, and 1.3 million
deaths in India per year.
• 80% deaths CVD, and > 60% from indoor air pollution.
• Air pollution rivals the effects of hypertension, smoking, or physical inactivity.
• 95% of the urban population currently lives in cities where the levels of air
pollution
11/4/2018 4Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
7. Composition of Air Pollution
• Air pollution consists of aerosols containing a mixture of both particles and gases
• Particulate matter (PM) is easily measured and readily relatable to the adverse
health effects
• PM stands for particulate matter (also called particle pollution)
• mixture of solid particles and liquid droplets found in the air
• PM10 : inhalable particles, with diameters that are generally 10 micrometers and
smaller
• PM2.5 : fine inhalable particles, with diameters that are generally 2.5 micrometers
and smaller.
11/4/2018 7Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
17. Gaseous Pollutants
• Generated by burning of fossil fuels or industrial processes, agriculture, volcanic eruptions
• Secondary pollutant gases are generated by atmospheric chemistry-mediated by sunlight,
water, and vapor.
• Pollutants such as hydroxyl radical, peroxyacetyl nitrate, nitric acid, formic acid, and acetic
acid, as well as formaldehyde and acrolein, arise from such atmospheric reactions
11/4/2018 17Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
18. Outdoor and Indoor Air Pollution
• PM generated by both natural and anthropomorphic sources.
• Processes such as volcanic eruptions, spontaneous forest fires, sea sprays, and soil erosion are
natural unpaved roads, traffic, mining, welding, building and other human activities.
• Most coarse PM (PM10) arises from dust and ground materials, endotoxin, pollen grains,
fungal spores, vegetation, and debris, whereas fine PM (PM2.5) is derived mostly from smog,
traffic, and combustion.
• In most urban environments, traffic is the major source of PM
• Combustion of any fossil fuel wood, gas, diesel, and gasoline—generates PM, particularly
fine and ultrafine PM.
11/4/2018 18Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
23. Outdoor and Indoor Air Pollution
• Developing countries, indoor air pollution from biomass fuels, coal, and kerosene burned
• Cooking, particularly frying, is an important source of indoor pollution.
• Cooking indoors can lead to a 10-fold increase in the number of ultrafine particles
• Burning of candles or incense can generate high levels of particulate air pollution.
• Air fresheners generate xylene, aldehydes, and esters, which can react with O3 to produce
secondary pollutants
• Pollen, dander, toxic molds, and dust, which frequently consists of fungi, endotoxin and
bacteria, as well as tobacco smoke
11/4/2018 23Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
24. Outdoor and Indoor Air Pollution
• There are few indoor sources of PM2.5, which comes mostly from outdoor sources and traffic
• Living next to a major street increases the levels of indoor PM2.5 and increases exposure to
traffic-generated pollutants such as NOx and VOCs.
11/4/2018 24Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
26. Pathophysiology
• Ambient air particles (<10 μm) results in the deposition of airborne particles in the lung,
• PM10 is deposited in the bronchial airways, activates the innate immune response
• Production of interleukin (IL)-8
• Recruitment of neutrophils to the lung leads to airway inflammation.
• Fine particles are deposited in lung, especially in the alveoli, also pass into circulation.
• Impaired surfactant function could lead to chronic lower airway inflammation
• UFP pass from the lung to other peripheral organs, including the heart and the brain
11/4/2018 26Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
27. Pathophysiology
• Production of reactive oxygen species (ROS)
• Decrease in lung capacity and pulmonary inflammation
• Accumulation of neutrophils, protein and fibrinogen in the bronchoalveolar fluid
• Inducing apoptosis in alveolar macrophages
• Inhibiting PMN phagocytosis and respiratory bursts
• Mild pulmonary inflammation, the systemic consequences of which exacerbate CVD risk.
• PM inhalation directly activates sensory receptors
• Imbalance in the autonomic nervous system, which may affect both cardiac rhythm and
cardiac conduction, leading to an increase in the risk of arrhythmias and SCD, particularly in
vulnerable individuals
11/4/2018 27Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
29. Cardiovascular Effects of Air Pollution
11/4/2018 29Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
30. Air Pollution and Cardiovascular Mortality
• 80% of deaths attributable to chronic air pollution are CVD
• Particularly IHD, arrhythmias, heart failure, and cardiac arrest
• 10μg/m3 increase in PM2.5 levels is associated with 8% -18% excessive risk of CV mortality
• No threshold has been detected below which air pollution does not affect CV health
• The exposure-response relationship between long-term exposure to PM2.5 and the risk of
CVD mortality steep at low levels of exposure and flattening at high exposure levels, such
that most of the risk is imparted at low levels of exposure
• Risk of CVD mortality caused by long-term PM2.5 exposure may be comparable in different
cities, even with widely different levels of air pollution.
11/4/2018 30Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
31. Air Pollution and Cardiovascular Mortality
• Short-term increases in PM are associated with increased risk of total mortality.
• 10μg/m3 increase in PM2.5, 0.7% to 1.7% increase in all-cause mortality on subsequent days
• Relationship between PM exposure and mortality independent of gaseous co-pollutants
• Smokers, elderly persons, and diabetes or heart failure particularly sensitive to PM exposure.
11/4/2018 31Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
32. Air Pollution and Cardiovascular Mortality
• Indoor exposure to air pollution is also linked to excessive CV mortality.
• In developing countries, indoor air pollution caused by biomass burning is associated with 2
million deaths per year
• Use of biomass fuels for cooking and heating increases the risk of coronary heart disease
(CHD) twofold to fourfold
11/4/2018 32Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
33. Myocardial Infarction
• Both acute and chronic exposures increase risk
• Elevated risk for MI with exposure to elevated PM or traffic exposure (1, 2, or 6 hours or a
few days)
• The acute risk may remain elevated and may increase even 2 days after exposure
• 10% to 20% increase in risk per 10μg/m3 increase in PM2.5 levels
• The risk is more strongly associated with PM2.5
11/4/2018 33Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
34. Myocardial Infarction
• Mostly to elderly individuals or those with CAD or structural heart disease.
• Obese women may be particularly at risk.
• associated with the risk of STEMI NOT NSTEMI
• Long-term exposure to traffic-related air pollution is also associated with MI recurrence.
11/4/2018 34Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
35. Arrhythmogenesis
Cardiac electrical instability,
Alterations in heart rate
Heart rate variability
Increase arrhythmia risk
Individuals with preexisting disease are likely to be more sensitive.
Decrease in parasympathetic tone
QT prolongation
intraventricular conduction delay
dispersion of ventricular repolarization
11/4/2018 35Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
36. Arrhythmogenesis
• Increase the risk of atrial fibrillation (AF) as
• prolongation of the PR duration
• Increase in the P wave complexity
• increase in the daily maximum heart rate
• Heart block frequency
• Percentage of time in AF
• Episodes of paroxysmal AF detected by ICDs are
• Higher risk of AF and ventricular tachycardia.
• Increase the risk of sudden cardiac death (SCD) and fatal CHD
11/4/2018 36Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
37. Arrhythmogenesis
• Risk higher in elderly persons or individuals who have underlying cardiac disease.
• Strongest for PM10, PM2.5, and O3, a well as traffic-generated pollutants.
• In patients with ICD, even moderate increases in air pollution appear to be associated with
ventricular arrhythmias within 2 hours of exposure
• Ambient levels of PM2.5 increased risk of out-of-hospital cardiac arrest, particularly in
individuals with high CVD risk burden
11/4/2018 37Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
38. Heart Failure
Increase in daily hospitalization for HF
Increase in HF admissions
Direct effects of chronic exposure to air pollution on cardiac function and
remodeling have been reported in both human and animal studies
air pollution are associated with increased right and left ventricular mass
11/4/2018 38Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
39. Hypertension
• Acutely with changes in systemic arterial BP (approximately 1 to 4 mm Hg per 10μg/m3
increase in PM)
• Effects larger in elderly individuals or those with preexisting CVD
• Chronic exposure to elevated levels of air pollution may lead to the onset of hypertension
• Individuals who live near major roadways and are therefore exposed recurrently to traffic-
generated pollutants have a higher prevalence of hypertension
• Comparing those who live less than 100 m of a major roadway with those who live more than
1000 m, a 9% higher prevalence has been reported
11/4/2018 39Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
40. Hypertension
• Acute exposure to PM or diesel exhaust could lead to a modest (3 to 4 mm Hg), but rapid
increase in systolic BP and a smaller increase in diastolic BP.
• Significantly, antihypertensive drugs appear to mitigate against the effects of air pollution on
BP, and therefore appropriate medical management of hypertension could attenuate the impact
of air pollution exposure.
11/4/2018 40Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
41. Hypertension
• indoor air pollution increases systolic, and to a lesser extent, diastolic BP.
• may be significant in individuals with preexisting disease.
• Indoor air pollution due to the use of solid fuels is also associated with increased
prevalence of hypertension
11/4/2018 41Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
43. Management and Intervention
Difficult to control at an individual level.
Exposure can be reduced by individual choices to diminish the impact of air pollution on CV
health. avoidance of areas of high pollution, especially traffic pollution, particularly by
individuals with high CVD risk.
Because residential proximity to major roadways increases exposure to traffic pollutants,
avoidance of such exposure may be particularly beneficial for post-MI patients or those with
HF.
11/4/2018 43Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
44. Management and Intervention
• Most indoor pollutants (e.g., molds, endotoxin, bacteria, dust) can be eliminated by
maintaining clean living environments
• Avoiding the use of candles, incense, or air fresheners indoors.
• Discontinuing the use of solid biomass for fuel
• using chimney woodstoves that prevent the accumulation of indoor air particulates
11/4/2018 44Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
45. Management and Intervention
• Exposure to particles generated by cooking and frying can be minimized by proper ventilation
or filtration.
• Most airborne particles can be removed by an electrostatic precipitator in a single-pass
efficiency of 90% or greater, even for smaller particles.
• Vehicle air conditioning can reduce exposure to traffic-generated air pollutants
• Eliminating tobacco smoke might have the most robust effect on improving indoor air quality.
11/4/2018 45Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
46. Take home message
• 80% deaths CVD, and > 60% from indoor air pollution
• Particularly IHD, arrhythmias, heart failure, and cardiac arrest
• Most indoor pollutants can be eliminated by maintaining clean living environments
• Residential proximity to major roadways increases exposure to traffic pollutants
11/4/2018 46Braunwald Heart disease, 11th edition, Chapter 52 Air Pollution and Cardiovascular Disease
