Understanding Heart Disease Statistics

The Numbers

• About 702,880 Americans died from heart disease in 2022, approximately 1 in every 5 deaths.
• Coronary heart disease is the most common type of heart disease and killed over 375,476 people in 2021.
• Approximately 20.1 million adults age 20 and older have CAD.
• Heart disease is the leading cause of death for both men and women among most racial and ethnic groups in the US.
• Heart disease costs the United States $252.2 billion each year from 2019-2020, including health care, medications, and lost productivity due to death.
• Heart disease is the leading cause of death for people of most racial/ethnic groups in the USA, including African Americans, America Indian, Alaska Native, Hispanic, and White men.
• For women of Asian American or Pacific Islander, American Indian, Alaska Natives, or Hispanic descent, heart disease is second only to cancer.

Total Cholesterol

• Total Cholesterol measures LDL, HDL, and other lipid components.
• A desirable level is <200 .
• Borderline high is between 200-239.
• High level is 240>.
• LDL:HDL Ratio provides a composite risk marker.
• A ratio of < or = 3:1 indicates decreased risk.
• A ratio of > or = 5:1 indicates increased risk.
• Total Cholesterol (CHOL):HDL Ratio is the best predictor for development of cholesterol related blockages.
• A value >4.5 indicates an increased risk of atherosclerosis.

Pathogenic Mechanism of Plaque Formation

• The earliest detectable atherosclerotic lesion is known as the fatty streak (lipid foam cells).
• Fatty streak ? fibrous plaque.
• The first lesion appears as a result of atherogenesis, possibly in early teen years, and consists primarily of foam cells in the subendothelial space.

Myocardial Ischemia

• Myocardial Ischemia occurs when myocardial oxygen demand is greater than the supply.
• It's reversible.
• Increased oxygen demand causes exercise, mental stress and spontaneous fluctuations of Heart Rate or Blood Pressure.
• Decreased oxygen supply causes decreased coronary blood flow.
• Myocardial Ischemia is diagnosed by exercise stress test, arrhythmias and T wave inversion on an EKG later becoming ST elevation.

Chronic Stable Angina

• Usually associated with a set level of O2 demand.
• It usually lasts several minutes.
• Precipitated by exertion (sometimes see term "exertional angina"), emotional stress and heavy meals.
• Symptoms in addition to pressure and heaviness may include dyspnea on exertion (DOE), fatigue, weakness, and syncope (may hear term anginal equivalents).
• Symptoms may be relieved with nitroglycerin (NTG).

Unstable Angina

• Angina symptoms occur without the demands that usually provoke it.
• Change in typical pattern or symptoms occurs at rest (without Oxygen demand).
• Possible evidence: complex coronary stenosis, plaque rupture, plaque ulceration, and hemorrhage and thrombus formation.
• The situation may progress to complete occlusion and infarction.

Prinzmetal's Angina (Variant or Atypical Angina)

• Occurs almost exclusively at rest due to coronary artery spasm.
• Angina can be severe, awakening patients from sleep.
• Spasm responds to NTG sometimes.
• It usually involves the RCA.
• Associated with arrhythmias ans conduction defects (VT and V-fib) and acute MI.
• Silent (Asymptomatic) Ischemia.

Myocardial Infarction (MI)

• Infarction leads to complete interruption of blood supply to an area of the myocardium and sudden arterial (or venous) insufficiency.
• This produces an area of necrosis and develops from ischemia.

Causes of MI

• Prolonged myocardial ischemia is usually due to plaque rupture/thrombus formation.
• Prolonged vasospasm and insufficient blood flow (decreased BP) or excessive metabolic demand is a less frequent cause.
• Embolic occlusion, aortitis, vasculitis or coronary artery dissection is rarer cause.
• Cocaine and other stimulants may lead to severe vasoconstriction resulting in MI.
• MI leads to focal death of myocardial tissue in the area supplied by the involved coronary artery and is very often in the LV.

Response to MI

• Necrotic tissue cells die and refer to the zone off infarct.
• 18-24 hours after MI, an inflammatory response to necrosis occurs.
• 2-4 days after MI, visible necrosis present, myocardial recovery begins.
• 4-10 days after MI, debris is cleared, and the matrix laid down.
• 10-14 days after MI, formation of a weak fibrotic scar and revascularization occurs.
• Scar tissue is inelastic and unable to contract and relax like healthy myocardial tissue.

MI Classification

• Subendocardial is a partial thickness and NSTEMI or Non-Qwave MI.
• An acute injury to the myocardium does not extend through the full thickness of the wall, but its EKG shows ST-segment depression with NO Q wave.
• Transmural is a full thickness, STEMI or Q wave MI.
• Full thickness injury extending through the entire wall of the muscle.

Newer Classification of MIs

• Type 1 is due to acute coronary atherothrombotic myocardial injury with either plaque rupture or erosion, and can be both STEMI and NSTEMI.
• Type 2 is where the reason for Myocardial Ischemia is due to oxygen supply-demand imbalance for reasons other than atherothrombotic injury.

Diagnosis of MI

• At least 2/3 of these must be present: Anginal Symptoms, EKG Changes and Rise of Cardiac Enzymes.
• Anginal Symptoms include chest pressure, heaviness, pain, arm, jaw, DOE, fatigue, syncope, belching.

Women's Symptoms Sometimes Differ

• Women are slightly more likely than men to report unusual symptoms.
• A multi-center study of 515 women who had an acute myocardial infarction (MI), the most frequently reported symptoms were unusual fatigue, sleep disturbances, shortness of breath, indigestion and anxiety.
• The majority of women (78%) reported at least one symptom for more than one month before their heart attack.

Silent Myocardial Infarction

• No angina symptoms.
• Can occur in any patient but more common in those with DM and EtOH abuse and peripheral neuropathies may contribute to this.
• Ruled in by EKG changes and Cardiac Enzymes.

Cardiac Enzymes: Troponin

• The preferred marker is Troponin (2004).
• There are different types of Troponins: Troponin I and Troponin T.
• Troponin released to the blood during MI.
• It elevates between 4-6 hours after MI, remains elevated for days (longer than CK – MB) and peaks at 24 hours.

Cardiac Enzymes: CK-MB and Myoglobin

• Creatine Kinase is released when cells die.
• Elevated during MI, specific for myocardial cell necrosis and returns to normal in 2-3 days.
• Peak elevations occur during the first 24 hours and lead to more false results.
• Myoglobin, a protein released with injury to the myocardium, elevates within 1-4 hrs but gives good results, if patients get to ER quickly.

Diagnosis of Acute MI: Additional Tests

• CXR, not specific for an MI.
• TEE: Transesophageal Echocardiogram.
• Coronary Angiography (Angiogram).
• Cardiac Catheterization, to rule MI in and used as a treatment option.

Medical Treatment of MIs

• Pharmacological Agents reduce myocardial oxygen demand, including Beta Blockers and Calcium Channel Blockers.
• Agents also increase myocardial oxygen supply like Vasodilators (Nitroglycerin).
• Pharmacological Agents also improve myocardial muscle function like Digitalis Glycosides.

Surgical Treatment of MIs

• Thrombolysis.
• Intra-aorta Balloon Pump (IABP).
• Percutaneous Transluminal Coronary Angioplasty/Percutaneous Coronary Intervention (PTCA/PCI), which can be with or without Stent Placement.
• Coronary Artery Bypass Graft (CABG).
• Left Ventricular Assist Device (LVAD).
• Cardiac Transplantation.

Cardiac Muscle Pump Dysfunction vs Failure

• Cardiac Muscle Pump Dysfunction produces small cardiac impairment, seen by small decreases in SV, CO, and EF and has less marked functional effects.
• Cardiac Muscle Pump Failure means Cardiac muscle fails to contract/relax enough which results in significant decreases in SV, CO, and EF and exercise causes myocardial ischemia.
• Heart chambers and pulmonary artery pressures increase in both dysfunction & failure.

Congestive Heart Failure (CHF)

• CHF is a syndrome where the heart is unable to pump enough output to meet the body's metabolic demands.
• CHF may result from any structural/functional cardiac disorder that impairs the filling ability or the pumping mechanism of the ventricles.
• Risk Factors include CAD, HTN, DM, Valvular and congenital heart disease, Arrhythmias, ETOH/drug abuse, and Age.

Characteristics of CHF

• Dyspnea.
• Tachypnea.
• PND.
• Orthopnea.
• Fatigue.
• Peripheral edema and cyanosis.
• Weight gain and hepatomegaly.
• Jugular Vein Distention.
• Rales/crackles (esp wet).
• S3 heart sound.
• Sinus tachycardia.
• Poor exercise tolerance.

CHF classification

• Systolic vs Diastolic Heart Failure
• Left Sided/Ventricular Failure vs Right Sided/Ventricular Failure
• Heart Failure with Reduced Ejection Fraction (HFrEF) vs Heart Failure with Preserved Ejection Fraction (HFpEF)

Systolic Heart Failure

• Decreased contractility leads to pump failure and is the most common problem associated w/heart failure.
• Increased preload leads to pump failure.
• Increased afterload leads to pump failure.
• Changes in Chronotropy where the heart rate is too slow or too rapid leads to pump failure.

Diastolic Heart Failure

• It may be impaired due to excessive hypertrophy of ventricles and/or changes in composition of myocardium.
• End Diastolic Volume (EDV) is decreased due to decrease filling of the left ventricle and increased stiffness.
• Decrease in compliance of the left ventricle increases the ventricular pressure at any given EDV.
• It leads to decreased cardiac output and overall elevated diastolic pressures.

Edema due to CHF

• Pulmonary and/or Systemic Edema results from heart failure because increased EDV gets transmitted back up to the atria and to venous circulation.
• It can lead to increased pulmonary capillary pressure which then leads to transudation of fluid causing pulmonary &/or systemic edema.
• Pressure in pulmonary vasculature where pulmonary edema develops is ~25 mmHg.

Left Sided/Ventricular Failure: CHF

• Inability to pump well causes decreased Stroke Volume and Cardiac Output, increased Left Ventricular End Diastolic Volume and decreased Left Ventricular compliance.
• Left ventricle dysfunction also leads to increased left atrial dilatation, increased pressure in pulmonary vessels & transudation of fluid from pulmonary capillaries.
• Increased Left Ventricular End Diastolic Pressure (pressure).
• Stretching of the mitral valve annulus leads to mitral valve regurgitation from LV dilatation.

Right Sided/Ventricular Failure: Cor Pulmonale

• Prolonged pulm HTN increases right ventricle afterload with anatomical changes (dilatation with possible hypertrophy) to the right ventricle that increase Right Ventricular End diastolic Pressure.
• All the right ventricular problems reflect back up to right atrium and venous system.

HFrEF vs HFpEF

• HFrEF (Heart failure with reduced ejection fraction) most frequently associated with heart failure and is the result of low CO at rest/with exertion.
• HFpEF (Heart failure with preserved ejection fraction) usually results from volume overload, is still of lower CO even though "preserved".

Cardiac/Ventricular Remodeling

• Refers to changes in size, shape, structure and physiology of the heart after injury (MI, chronic HTN).
• There are both structural and functional changes that occur in zones (infarction, injury, ischemia).
• Begins minutes after MI and continues over time.
• The left ventricle may change from elliptical to spherical.
• Apoptosis is a programmed death of cells.

Ventricular Remodeling (Definition)

• Ventricular size (usually left) increases, the heart becomes more spherical and mitral regurgitation.
• Ultimately systolic performance worsens.

Physiologic Consequences of CHF

• Decreased myocardial performance tries to increase venous return w/peripheral vascular constriction, increased peripheral vascular resistance as a consequence.
• Increased sympathetic stimulation in the heart desensitizes heart to Beta 1-adrenergic stimulation and decreases heart's inotropic effect(contractility).
• Pulmonary edema develops due to increased filling pressures.
• Decreased cardiac output decreases renal blood, glomeruler filtration rate, sodium and fluid retention, vasopressin production.
• Muscle wasting and potential skeletal muscle myopathies occur with exercise.

Compensation for CHF: SNS

• Decreased CO sensed by baroreceptors leads to increased SNS activity.
• The release of norepinephrine causes to increased HR, myocardial contractility, stroke volume, systemic resistance and BP.
• Peripheral vasoconstriction stimulates the kidneys to increase renin release.

Compensation for CHF: RAAS

• RAAS maintains BP and CO in the setting of volume depletion.
• It increases venous and atrial tone.
• It increases retention of salt and water.
• Release of renin in the system.
• Angiotensin II is a powerful vasoconstrictor that initially restores BP but, in the long run, leads to less CO, causes decrease in renal perfusion and contributes to remodeling.
• It promotes the release of aldosterone made in the adrenal gland that acts on the kidneys.
• The Review of Hormones Involved in CHF(not all-inclusive): Norepinephrine, Renin, Angiotensinogen and Aldosterone contribute to the disease process, with concentrations that correlate with severity and prognosis.

Counter-regulatory Hormones in CHF

• Natriuretic peptides (NP): ANP is atrial NP and BNP is brain NP.
• C type NP (endothelial) contributes to vasodilation.
• ANP and BNP get released when high filling pressures stimulate.
• Release also occurs during systemic and renal Sympathetic activity when Inhibit the RAAS.
• Natriuretic peptides also contributes to vasodilation (antihypertensive).
• NPs increase excretion by kidneys.

NYHA: Classification of CHF

• Classifies heart failure according to severity of symptoms.
• Functional classification places patients in one of four categories based on how much they are limited during physical activity.

Treatment of CHF

• Treatment is directed at the underlying cause.
• Goals involve improving the ability to pump and controlling sodium and water.
• Management includes non-drug, medical, and surgical options.

Medical management of CHF

• Goals are to decrease venous return & workload of heart and increase work of heart.
• Interventions include diuretics, vasodilators, digitalis (digoxin), Beta-Blockers, ACE (angiotensin converting enzyme) Inhibitors, inotropes, cholesterol-lowering drugs, and Aspirin.
• Hemodialysis/ultrafiltration may also be necessary.

Surgical management of CHF

• Cardiac resynchronization therapy (Pacemaker) can treat CHF.
• Other procedures encompass angioplasty with/without stenting, athrectomy, rotobladder, bypass, laser, IABP(intra-aortic balloon pump), ventricular assistive device, heart transplan and artificial heart.

Dilated Cardiomyopathy (DCM)

• Increased cardiac mass & dilatation of all 4 cardiac chambers, with little or no wall thickening & systolic dysfunction.
• Results in Decreased stroke volume and Impaired ability to increase with exercise.
• Dilated CM can be from Idiopathic causes, Heart disease, Uncontrolled HTN, Myocarditis infection/non-infection, Toxins, pregnancy, metabolic or hereditary disorders.
• Presents with dyspnea, fatigue, ventricular dysrhythmia of decreased O2.
• Good prognosis WITHOUT further clinical indication.

Hypertrophic CM (HCM)

Results in left ventricular hypertrophy impairs filling.

• The Normal Systolic function and NO cavity dilatation is the characterized by hypertrophic CM (HCM).
• Usually is not found until a routine medical examination.
• The first symptom may be sudden collapse