Heart failure/valve disorders

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Questions and Answers

What major change occurs in the ventricles when there is long-term increased afterload?

Improved compliance due to relaxation

Increased contractility of myocytes

Hypertrophy leading to increased wall thickness (correct)

Decreased wall thickness and chamber size

Which characteristic of a normal ventricle is compromised in heart failure?

Ability to generate force (correct)

Diastolic filling at low atrial pressures

Quick release and re-sequestration of calcium

Ability to maintain a significant reserve of function

In the context of heart failure, what does impaired oxygen supply refer to?

Chronic ischemic heart disease impacting myocardial function (correct)

Increased blood flow to the myocardium

Enhanced contractility of the ventricular walls

Significant hypertrophy of the atria

How do cardiomyopathies affect the heart's function?

They damage the myocardium impairing both compliance and contractility Signup and view all the answers

What distinguishes HFpEF from HFrEF?

HFpEF is characterized by diastolic dysfunction, whereas HFrEF involves systolic dysfunction Signup and view all the answers

What is one of the potential consequences of reduced ventricular compliance?

Increased end-diastolic pressure Signup and view all the answers

What is a common clinical feature of aortic regurgitation?

A diastolic murmur heard best at the right second intercostal space Signup and view all the answers

Which of the following correctly describes a feature of hypertrophic cardiomyopathy?

It may lead to outflow obstruction under exertion Signup and view all the answers

What is primarily responsible for about 2/3 of heart failure cases?

Atherosclerosis alone Signup and view all the answers

What characterizes systolic dysfunction in heart failure?

Impaired force of contraction Signup and view all the answers

Heart failure with preserved ejection fraction (HFpEF) is mainly characterized by which of the following?

Increased diastolic pressures Signup and view all the answers

Which tissue is least likely to experience decreased perfusion during heart failure?

Skeletal muscles Signup and view all the answers

What condition can develop due to elevated pressures in pulmonary capillaries during congestive heart failure?

Pulmonary edema Signup and view all the answers

What defines the 'backsward' problems associated with heart failure?

Congestion in systemic venous circulation Signup and view all the answers

As the left ventricle struggles with higher afterloads, which other ventricle is primarily affected next?

Right ventricle Signup and view all the answers

In the context of heart failure, what is often observed in the lungs due to increased left ventricular afterload?

Pulmonary hypertension Signup and view all the answers

What is NOT typically a consequence of decreased cardiac output in heart failure?

Improved perfusion to the heart Signup and view all the answers

Which factor does NOT contribute to the development of right ventricular failure?

Elevated systemic arterial pressure Signup and view all the answers

What is the most common cause of mitral stenosis?

Rheumatic heart disease Signup and view all the answers

What are the characteristic symptoms of aortic stenosis?

Chest pain and syncope Signup and view all the answers

Which valve is least likely to be affected by rheumatic fever in terms of frequency?

Pulmonary valve Signup and view all the answers

What complication can arise from chronic rheumatic heart disease (RHD)?

Incompetent valves Signup and view all the answers

What is the common prognosis for aortic stenosis if left untreated and resulting in left ventricular hypertrophy (LVH)?

Common cause of congestive heart failure (CHF) Signup and view all the answers

Which clinical feature is the main cause of morbidity and mortality associated with rheumatic fever?

Carditis Signup and view all the answers

What type of murmur is typically heard with aortic regurgitation?

Diastolic decrescendo Signup and view all the answers

What is a common consequence of myocardial pressure overload due to aortic stenosis?

Left ventricular hypertrophy (LVH) Signup and view all the answers

What is the primary cause of aortic regurgitation in older patients?

Surgery for aortic stenosis Signup and view all the answers

What percentage of the population is affected by mitral valve prolapse?

2-3% Signup and view all the answers

Which condition is associated with an increased risk of aortic stenosis?

Bicuspid aortic valves Signup and view all the answers

What is a common prevalence rate of moderate aortic regurgitation in older patients?

2% Signup and view all the answers

What is the pathogenesis similarity between calcific aortic stenosis and atherosclerosis?

Both involve endothelial damage and inflammation Signup and view all the answers

How does mitral valve prolapse typically affect the heart's structure?

Increases valve leaflet thickness Signup and view all the answers

In which condition do myofibroblasts differentiate into bone-like cells?

Aortic stenosis Signup and view all the answers

What percentage of congenital heart diseases are due to congenital bicuspid aortic valves?

5% Signup and view all the answers

Which of the following is a contributing factor to acute damage of the aortic valve?

Thoracic aortic dissection Signup and view all the answers

What common symptoms might you expect in a patient with significant aortic stenosis?

Dyspnea, angina, and syncope Signup and view all the answers

What is a common symptom associated with mitral valve prolapse?

Palpitations Signup and view all the answers

Which type of murmur is typically associated with mitral regurgitation?

Holosystolic murmur Signup and view all the answers

What is the prognosis for patients with asymptomatic mitral valve prolapse?

Most have a good prognosis Signup and view all the answers

Which murmur is best heard at the apex and follows an 'opening snap' in mitral stenosis?

Rumbling diastolic murmur Signup and view all the answers

In which scenario is surgery more urgently needed for mitral regurgitation?

When LVH develops and symptoms appear Signup and view all the answers

What common symptom might worsen with exercise or activity in patients with mitral stenosis?

Dyspnea Signup and view all the answers

What condition is often indicated by the presence of a mid or late-systolic click in patients with mitral valve prolapse?

Mitral valve prolapse Signup and view all the answers

What type of murmur might be difficult to hear in cases of severe mitral regurgitation?

S1 heart sound Signup and view all the answers

What is the primary result of pulmonary vasoconstriction in the context of hypoxic conditions?

Decreased blood flow to the lungs Signup and view all the answers

What distinguishes eccentric hypertrophy from concentric hypertrophy in heart failure?

The chamber size increases with thinner walls Signup and view all the answers

What happens to calcium homeostasis in the failing heart?

Diastolic calcium levels are elevated Signup and view all the answers

Which factor is NOT associated with maladaptive remodeling of the heart?

Activation of IGF-1 pathways Signup and view all the answers

Which of the following best describes the hemodynamic change that occurs due to Angiotensin II in heart failure?

Increased volume retention and vasoconstriction Signup and view all the answers

What characterizes the differences between HFrEF and HFpEF?

HFrEF is typically associated with increased wall thickness Signup and view all the answers

Which pathway is implicated in sodium and water retention in heart failure?

Activation of the RAAS Signup and view all the answers

During HF, which pattern is primarily associated with an increase in wall stress?

Concentric hypertrophy without change in chamber size Signup and view all the answers

Which change occurs in beta-adrenergic signaling during prolonged heart failure?

Downregulation of receptors leading to decreased efficacy Signup and view all the answers

What is the consequence of signaling pathways activated by inflammatory cytokines in heart failure?

Maladaptive remodeling Signup and view all the answers

What is a common symptom associated with left-sided heart failure?

Dyspnea Signup and view all the answers

Which clinical feature is typical for a patient classified in New York Heart Association Class II?

Comfortable at rest, but normal activities cause fatigue Signup and view all the answers

How does the structural adaptation in the failing heart affect the capillary network?

Reductions in capillary density compared to physiological hypertrophy Signup and view all the answers

What effect does SERCA inhibition have in heart failure?

Increases diastolic calcium and compromise contraction Signup and view all the answers

Study Notes

BMS 200 - Cardiology 6

Study topics include heart failure, cardiomyopathies, and valvular heart disease.

Outcomes

Describe general pathologic findings and pathophysiology of valvular stenosis, regurgitation, and prolapse.
Relate valvular disease pathophysiology to physical exam findings.
Describe epidemiology, pathogenesis, clinical features, and prognosis of aortic regurgitation, calcific aortic stenosis, bicuspid aortic valves, mitral valve prolapse, mitral regurgitation, and rheumatic heart disease.
Describe epidemiology, pathogenesis, clinical features, and prognosis of hypertrophic cardiomyopathy, dilated cardiomyopathy (hereditary), and restrictive cardiomyopathy. Also describe CAD-related ventricular failure and hypertensive heart disease.
Relate cellular and gross pathophysiologic adaptations in heart failure to underlying etiologic and risk factors.
Compare pathogenesis, clinical features, diagnostic findings, and complications of left-sided and right-sided congestive heart failure.
Compare the pathogenesis, clinical features, diagnostic findings, and complications of HFpEF and HFrEF.
Briefly describe the pharmacologic mechanism of action and related adverse effects of common medications used to treat heart failure.

Heart Failure - Introduction

A normal ventricle should be compliant, allowing filling at low atrial pressures, without needing hypertrophy.
The ventricle should relax quickly, with most filling happening in early diastole.
"Strong" ventricles generate enough force at rest, even with low preload to meet the body's needs.
Calcium should be quickly released and re-sequestered each cycle.
There's a reserve of function in response to increased activity.
Heart failure can result from increased afterload, causing ventricular hypertrophy and increasing wall thickness. Molecular changes lead to decreased contractility.
Heart failure can involve ischemic heart disease, with or without infarcted tissue, or impaired relaxation that results in reduced compliance. Molecular and other poorly defined changes are also factors.
Heart failure can result from cardiomyopathies, disorders that damage myocardium causing a loss of compliance or contractility.

Heart Failure - Prevalence

Prevalence of heart failure in US adults 20 years or older changes by gender and age.
Major underlying etiologies/risk factors for heart failure include valvular disease, LVH (left ventricular hypertrophy), hypertension, and diabetes among others. Specific percentages are noted but not consistent with 100%.
Atherosclerosis is a major contributor, responsible for about 2/3 of failure cases.

Heart Failure - P-V Loops

Heart failure pathogenesis has two primary phenotypes.
Systolic dysfunction involves impaired contraction/contractility with or without adequate cardiac output.
Diastolic dysfunction involves elevated diastolic pressures but with maintained contractility.

Heart Failure - P-V Loops (Continued)

Systolic dysfuntion is mostly referred to as HFrEF (heart failure with reduced ejection fraction.)
Diastolic dysfunction is mostly referred to as HFpEF (heart failure with preserved ejection fraction.)

Pathophysiologic pathways in CHF

Two main problems result from the progression of heart failure:
Forward flow problems (reduced cardiac output): causes impaired perfusion to tissues, organs, particularly brain, heart, kidneys, and extremities.
Backward flow problems (congestion): Blood congestion occurs in pulmonary venous circulation resulting in elevated pressures in pulmonary capillaries leading to pulmonary edema, thickened arterioles/arteries in the lung. Then blood congests in the systemic venous circulation from decreased right ventricle output resulting in increased pressures in systemic capillaries, leading to edema in various areas.
Congestion can also occur as a consequence of decreased left ventricular output. The right ventricle struggles to keep up with the needs of the body, leading to right heart failure. The most common cause of this is when the left side of the heart fails as afterload and preload issues develop. This can happen with issues like COPD and obstructive sleep apnea, and is known as cor pulmonale.

Pathophysiologic Pathways in CHF (Comparison of Microcirculation)

Pulmonary microcirculation adapts to decreased oxygen levels by constricting blood vessels. This differs from other vascular beds where reduced oxygen levels cause vasodilation.
This makes sense because reduced oxygen in the pulmonary system means that less blood needs to be delivered to the lungs in that location.

Pathophysiologic Pathways in CHF (Molecular Adaptations)

The structure of myocytes and surrounding tissue undergo changes (remodeling) over time.
Increased expression of fetal myosin types that effectively use ATP, but with less force; increased TGF-β.
Deposition of extracellular matrix material.
Capillary network is less extensive compared to physiologic hypertrophy.

Pathophysiology Pathways in CHF (Signaling Pathways)

Angiotensin II plays a role when cardiac output to the kidneys decreases: Increased ATII.
ATII can be released by stressed cardiac cells.
ATII directly binds to myocytes, increasing hypertrophy, proliferation of myofibroblasts. It increases connective tissue deposition.
Increased ATII leads to increased volume, vasoconstriction, and worsened edema and afterload.
Beta-adrenergic signaling increases in early heart failure.
Long-term beta signaling can result in hypertophy, fibrosis, and apoptosis of cardiomyocytes.
Some damaging pathways (like endothelin-1 and inflammatory cytokines) may be involved also in remodeling and apoptosis.
Calcium homeostasis is altered in failing hearts (ryanodine receptors release less calcium per action potential, and SERCA calcium uptake is inhibited).

CHF Pathophysiology & Neurohormonal Activation

Activation of the SNS and RAAS initially leads to increased heart rate, blood pressure, contractility, retention of sodium and water.
Increased preload and cardiac output.
Over time imbalances develop from excessive vasoconstriction and volume retention. Baroreceptors dysfuntion leading to elevated pressures, and decreased PNS tone.
Increased ADH release in response to decreased renal perfusion leads to chronically elevated renin release and activation of AT2, to help maintain blood flow to the kidneys.

RAAS - Review

RAAS model does applies when the kidneys release renin and AT2.
Renin release can be a response to decreased perfusion and activation of the SNS
RAAS model doesn't apply to cardiomyocytes releasing AT2.

Protection Against Fluid Overload

Both Atrial (ANP) and B-type natriuretic peptide (BNP) function similarly, being released by stretched ventricles.
BNP decreases blood volume through sodium and water excretion by kidney tubules.
Patients can become resistant to BNP and ANP over time.
Some medications (neprilysin inhibitors) can help reduce resistance.

Heart Failure - General Clinical Features

Symptoms are fatigue, orthopnea, dyspnea, angina, impaired cognitive function, dependent edema, hepatosplenomegaly, right upper quadrant pain, elevated jugular venous pressure, displacement of apical impulse, crackles, wheezing, and pleural effusions.

New York Heart Association Classification

This classification tool does not always correlate with objective measurements.
Class I: No limitation in ordinary physical activity.
Class II: Mild limitation; ordinary physical activity causes symptoms.
Class III: Marked limitation; less than ordinary physical activity causes symptoms.
Class IV: Severe limitation; symptoms even at rest.

Heart Failure - Diagnosis

Echocardiography is typically used.
HFrEF is diagnosed when ejection fraction (EF) is less than 40%.
HFpEF has a normal ejection fraction, typically greater than 50%.
More challenging to diagnose than HFrEF.
BNP is a natriuretic factor released by ventricles in response to increased strain.
Chest X-ray may help identify cardiomegaly and pulmonary edema.

Chronic IHD (Coronary artery disease) -> CHF

IHD is the most common cause of heart failure, accounting for roughly 60% of CHF cases.
Other contributing factors include hypertension, valvular abnormalities, and congenital heart disease.
Characterized by myocardial hypertrophy and fibrosis, presence of myocardial "scars," systolic and/or diastolic dysfunction, with left ventricle usually the first place of involvement.

Review - Atherosclerosis

Progression involves fatty streak to LDL deposit to macrophage migration/activation to calcification, cholesterol and foam cell development, extracellular matrix deposition under the intima, variable fibrous cap with underlying necrotic tissue, immune cells, stenosis, and blood flow impairment.

Review – Risk Factors & Atherosclerosis Development

Risk factors include: smoking, high blood pressure, oxidative stress that increase endothelial damage, increased LDL, inflammation at plaque site, immune response.
Risk factors also include elevated blood sugar linked to diabetes and dyslipidemia. Linked to metabolic syndrome, and resulting AGE's in the endothelium.

Chronic Hypertension -> CHF

Long-term hypertension commonly results in concentric left ventricular hypertrophy - increasing wall thickness but not chamber size.
Over time this can progress to eccentric hypertrophy.
Microscopy shows hypertrophied cardiomyocytes and increased capillary density.

Medications for CHF and/or Angina

Beta-blockers reduce heart rate and cardiac oxygen demand (especially useful in IHD and can also help in CHF remodeling with less fibrosis).
Cardiac glycosides increase contractility by raising intracellular calcium, but may also decrease heart rate through vagal effects, which can be a negative effect.
Diuretics decrease blood volume (especially sodium and water).

Mechanism of Action - Digoxin

Digoxin lowers the sodium gradient, reducing calcium extrusion from the cytosol. This produces a slight increase in calcium in the cytoplasm that improves contraction.

Medications for CHF (Diuretics)

Diuretics, especially loop and thiazide diuretics, work by inhibiting sodium reabsorption in the kidney tubules, leading to increased loss of water and sodium to reduce blood volume.
Spironolactone is a specific diuretic that blocks the aldosterone receptor to reduce sodium and water loss in the distal nephron.
ACE inhibitors (ACE-i) block the ACE enzyme that converts AT1 to AT2.

FYI - CHF Strategies

CHF is often related to multiple comorbid factors like IHD, hypertension, and diabetes that often require prevention as a means of treatment.

Medications for Angina (Calcium Channel Blockers)

Calcium channel blockers cause vasodilation with limited impact on cardiac conduction/contractility.
This can reduce oxygen demand, lowering workload.
Calcium channel blockers include dihydropyridines such as amlodipine and nifedipine.
Non-dihydropyridines such as verapamil or diltiazem to slow heart rate and cause vasodilation.

Dyslipidemia Medications (Basic MOA)

HMG CoA-reductase inhibitors (statins) reduce hepatocyte cholesterol production which increases LDL receptor expression. They lower circulating triglycerides and show less oxidative stress and inflammation at plaque sites.
PCSK9 inhibitors block PCSK9 enzyme that degrades the LDL receptor. More LDL receptors becomes available to clear excess LDL in the blood, thus lowering LDL.
Ezetimibe reduces cholesterol absorption in the small intestine to decrease cholesterol stores while increasing LDL receptors.
Niacin (less commonly used) decreases fatty acids in the liver, thus slowing VLDL production. This decreases circulating LDL but increases HDL.

Valvular Pathology - Generalities

Valves are composed of endocardium with dense irregular connective tissue, connected to fibrous rings.
Processes that damage valves include congenital issues, "wear and tear", inflammation (infection, autoimmunity), and acute impairments.
Examples include, bicuspid aortic valves, and conditions such as bacterial endocarditis, rheumatic fever, lupus, ankylosing spondylitis.

Review - Stenosis, Prolapse, Incompetence, Regurgitation

Stenosis is when the valve opening is narrowed, making it difficult and/or strenuous to open normally, leading to proximal wall hypertrophy.
Regurgitation is blood flow back across the valve, either due to incompetence or prolapse.
Prolapse is exaggerated valve movement backwards into the proximal chamber.
Incompetence (insufficiency) means the valve does not completely close, resulting in the flow of blood backwards.

Selected Valvular Pathologies - Today

The conditions discussed today include aortic regurgitation, bicuspid/calcific aortic stenosis, mitral valve prolapse and mitral regurgitation, and rheumatic heart disease.

Aorta - Aortic Stenosis/Sclerosis

Aortic stenosis is a very common condition in individuals 65 or older.
The progression commonly starts with aortic sclerosis, followed by asymptomatic aortic stenosis.
Congenital bicuspid aortic valves are frequently associated with aortic stenosis.
Congenital heart defects account for 1% of live births

Aortic Stenosis/Sclerosis - Pathogenesis

Calcific aortic stenosis has characteristics similar to atherosclerosis, including damage to the valvular endothelium, oxidative stress response (e.g. oxidized LDL and chronic macrophage inflammation).
Abnormal cell differentiation can accelerate the process.
Presence of a bicuspid aortic valve will expedite the condition's progression.
The effects of increased afterload include concentric hypertrophy of the heart.

Aortic Regurgitation

Aortic regurgitation is not as common as stenosis.
Significant aortic regurgitation has etiology related to stenosis conditions, especially where a valve fails to close fully, inflammatory disorders are frequent, as is acute damage to or dissection in the valve, potentially triggered by infective endocarditis.

Mitral Valve Prolapse

Mitral valve prolapse is the most common valvular abnormality, appearing in about 2-3% of the population.
The leaflets may be enlarged or redundant, and may prolapse into the left atrium during systole.
Microscopic examination reveals myxomatous connective tissue, with reduced collagen content.
The primary causes remain poorly understood, although some deficiencies in cadherins have been noted.
Secondary causes may include connective tissue disorders such as Marfan's syndrome.

Mitral Valve Regurgitation

Long standing mitral valve prolapse can result in mitral regurgitation, which occurs in about 15% of those with MVP.
Other causes of mitral regurgitation can include ischemia causing papillary muscle dysfunction, infective endocarditis, rheumatic fever, and left atrial/ventricle enlargement. Severe cases are frequently life-threatening.

MVP and MR

Acute mitral regurgitation can cause increased left atrial pressure, and pulmonary pressure.
Pathogenesis is complicated, including chordae tendinae rupture, or impaired/ ruptured papillary muscles.

Rheumatic Fever & Rheumatic Heart Disease

Rheumatic fever is an autoimmune disease following infection from group A streptococcus. A common cause of strep throat or skin infection (impetigo), the causative M-protein (of streptococcal antigens) causes the body's immune system to attack cardiac cells (valves), leading to heart damage/inflammation.
This reaction usually occurs about 2-3 weeks following infection.
RHD (Rheumatic Heart Disease) symptoms can take years to develop and can cause mitral, aortic, and tricuspid valve issues.

Chronic RHD - Valvular Disease

Mitral and aortic valves are frequently involved as well as damage to their supporting structure.
Most common findings as with mitral stenosis or aortic stenosis.
RHD most commonly leads to mitral stenosis.
Often the scarring and shorting of the chordae tendinae cause the valve to be more incompetent.
RHD can lead to fused aortic valve commissures (making them more like bicuspid).

Aortic Stenosis & Regurgitation

Symptoms of aortic stenosis are chest pain (if severe), syncope, and severe, sudden symptoms (if the heart's output is greatly hindered).
Signs of aortic stenosis include systolic crescendo-decrescendo murmur in the second right intercostal space. The murmur often radiates to the neck and is accompanied by apparent left ventricular hypertrophy.
Symptoms for aortic regurgitation are very dangerous if acute and severe, such as flash pulmonary edema, cardiogenic shock, and syncope. If untreated, significant aortic regurgitation can easily develop left ventricular hypertrophy (eccentric hypertrophy) that leads to heart failure.
Signs of aortic regurgitation include diastolic decrescendo murmur –can be hard to distinguish for left or right intercostal space, often sounding parasternally, bounding/water-hammer pulse with significant pulse pressure, loud S2 followed by a quiet S2.

Mitral Valve Prolapse & Regurgitation

Often asymptomatic with non-specific findings such as pre-syncope or palpitations.
Signs of mitral valve prolapse include mid or late systolic click followed by systolic crescendo (or crescendo-decrescendo) murmur.
If mitral valve regurgitation develops, more urgent surgical intervention to correct the condition may be necessary.
Significant or symptomatic left ventricular hypertrophy may develop.

Mitral Valve Stenosis

Often asymptomatic until atrial pressures become elevated.
Symptoms include cough and dyspnea, worsening with exertion.
Signs often include an opening snap and a rumbling, diastolic murmur at the apex.

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