Heart Disease Quiz

Cardiac Pathophysiology

• Cardiac pathophysiology is the study of the diseases and malfunctions of the heart.

• Coronary artery disease (CAD) is the leading cause of death in the US for both men and women across all racial and ethnic groups:

  • Approximately 702,880 Americans died from heart disease in 2022.
  • This accounts for about 1 in 5 deaths.
  • Coronary heart disease killed more than 375,476 people in 2021.
  • More than 20.1 million adults aged 20 and older have coronary artery disease (CAD).

• Heart Disease has a direct cost to the US healthcare system of $252.2 billion per year (2019-2020).

  • This includes costs of medical care, medications and lost productivity due to death.

• Heart disease is the most common type of disease among different racial/ethnic groups in the US.

  • For people of most racial/ethnic groups, it's the leading cause of death.
  • For women of Asian American or Pacific Islander, American Indian, Alaska Native, or Hispanic descent, heart disease is second only to cancer.

Objectives

• Explain the basics of coronary heart disease and how atherosclerotic plaques form.
• Identify types of angina.
• Understand myocardial infarction, including types and zones of infarction. How MI is diagnosed and the basic treatment.
• Differentiate between cardiac pump dysfunction and failure.
• Differentiate between right and left heart failure, as well as systolic and diastolic heart failure.
• Identify consequences of heart failure (CHF) and ventricular remodeling and how CHF is diagnosed.
• Describe types of cardiomyopathy, sudden cardiac death, aneurysms (including types), endocarditis, pericarditis.
• Describe cardiac tumors.

Pathophysiology

• Ischemic heart disease
  • Atherosclerosis/CAD/CHD
  • Angina
  • Myocardial Infarction (MI)
• Cardiac muscle dysfunction
  • Dyfunction
  • Heart failure
  • Cardiomyopathy
• Valve disease
  • Sudden cardiac death
  • Aneurysm
• Vascular disease
  • Endocarditis
  • Pericarditis
• Tumors

Coronary Heart Disease (CHD)

• "Build-up of plaque in the heart's arteries that can cause a heart attack."
• CAD: Coronary Artery Disease
• CHD: Coronary Heart Disease
• Terms are interchangeable; CHD is caused by CAD.
• Ischemia
• Infarction

Atherosclerotic Heart Disease (a.k.a. Coronary Artery Disease)

• Athero: gruel, soft deposit
• Sclerosis: hardening
  • Characterized by nodular deposits of fatty material lining artery walls (plaques).
  • Vessel walls lose elasticity and become sclerotic
  • "Hardening of the Arteries"

Risk Factors for CAD

• Lifestyles
  • Tobacco use
  • Diets high in saturated fat, cholesterol, and calories
  • Excess alcohol consumption
  • Lack of physical activity
• Biochemical/Physiologic Characteristics
  • Blood lipid abnormalities
  • High cholesterol
  • Elevated blood triglycerides
  • Hyperglycemia/diabetes (DM)
  • Obesity
  • Hypertension (HTN)
• Personal Characteristics
  • Gender (men are more affected)
  • Age (risk increases with age)
  • Family history of CAD
  • Personal history of CAD

Cholesterol

• Essential body compound needed for cell membrane structure and enzymatic activity. - Transports fatty acids and lipids
• Comes from two sources:
  • Our bodies (75%)
  • Food sources (25%, only from animal products)

LDL (Low-Density Lipoprotein)

• ("bad" cholesterol)
• Higher number = higher risk
• <100 desirable; 100-129 near optimal; 130-159 borderline high; 160-189 high; >190 very high
• <70 recommended for those with CHD or vessel disease; <100 recommended for those with DM or other risk factors

HDL (High-Density Lipoprotein)

• ("good" cholesterol)
• Higher number = lower risk

• 60 optimal; <40 (men), <50 (women) low

Triglycerides

• Also part of lipoprotein profile
• High level = high risk
• Fats carried in the blood from food we eat
• <150 normal; 150-199 borderline high; 200-499 high; >500 very high

Total Cholesterol

• A measure of LDL, HDL, and other lipid components
• <200 desirable; 200-239 borderline high; 240+ high
• LDL:HDL Ratio - Composite risk marker
  • < or = 3:1 ratio is ↓ risk

  • or = 5:1 ratio is an ↑ risk

• Best predictor for development of cholesterol-related blockages (>4.5 increased risk of atherosclerosis)

Myocardial Ischemia

• Occurs when myocardial oxygen demand is greater than supply.
• Reversible
• Increased oxygen demand caused by exercise, mental stress, spontaneous HR or BP fluctuations.
• Decreased oxygen supply caused by decreased coronary blood flow
• Diagnosed by exercise stress test (EKG showing arrhythmias and T wave inversion, later ST elevation).

Angina Pectoris (Angina)

• A classic symptom of ischemia
• Described as "pressure" or "heaviness"
  • Substernum (midchest)
  • Over the heart (precordial)
  • In the shoulder, arm, throat, or jaw
  • 2 types: chronic angina and unstable angina

Myocardial Infarction (MI)

• Complete interruption of blood supply to an area of the myocardium.
• Sudden arterial (or venous) insufficiency produces an area of necrosis.
• Develops from ischemia.

Causes of MI

• Prolonged myocardial ischemia (often from plaque rupture/thrombus formation)
• Prolonged vasospasm; inadequate myocardial blood flow (decrease BP or excessive metabolic demand)
• Less frequent cause: Embolic occlusion, aortitis, vasculitis or coronary artery dissection
• Rarer causes: Cocaine and other stimulants

Response to MI

• Cells die = necrotic tissue (zone of infarct)
• 18-24 hours post-MI: inflammatory response to necrosis
• 2-4 days: visible necrosis present, myocardial recovery begins
• 4-10 days: debris cleared, matrix laid down
• 10-14 days: formation of weak fibrotic scar, revascularization present

MI Classification

• Subendocardial (partial thickness): NSTEMI (Non-Q-wave MI)
  • Acute injury to the myocardium that does NOT extend through the full thickness of the wall
  • EKG: ST-segment depression with NO Q wave
  • May not have as significant EKG changes, but patient may be symptomatic and lab values indicate injury
• Transmural (full thickness) STEMI (Q-wave MI)
  • Full thickness injury extending through the entire wall of the muscle
  • EKG: ST-segment elevation, with significant Q wave indicates acute infarction.
  • ST returns to baseline in 24-48 hours

Newer MI Classification

• Type 1: Due to acute coronary atherothrombotic myocardial injury with either plaque rupture or erosion (can be both STEMI and NSTEMI)
• Type 2: Evidence of myocardial ischemia due to oxygen supply-demand imbalance for other reasons than atherothrombotic injury

Location of MI

• Depends on anatomic distribution of occluded vessel, more proximal a lesion, presence of additional chronic stenotic lesions, and collateral circulation
• Anterior wall: Left anterior descending artery (LAD)
• Lateral wall: Left circumflex artery (LCX)
• Inferior wall: Right coronary artery (RCA)

Diagnosis of MI

• At least 2/3 must be present: Cardiac symptoms, DOE, fatigue, syncope, belching.
• EKG changes (peaked T waves, ST elevation, Q wave presence, T-wave inversion)
• Rise in cardiac enzymes

Women's Symptoms in MI

• Women may report unusual symptoms (fatigue, sleep disturbances, shortness of breath, indigestion, anxiety) than men.

Silent MI

• No angina symptoms
• Often seen in patients with diabetes mellitus (DM) and/or alcohol use disorder (ETOH)
• Can be caused by peripheral neuropathies
• Diagnosed through EKG changes and cardiac enzymes

EKG Changes in MI

• Peaked T waves
• ST elevation
• Q wave presence
• T wave inversion

Diagnosis of MI - Cardiac Enzymes

• Cardiac muscle cells become necrotic.
• Cell necrosis leads to several cardiac markers diffusing into the blood including troponins, CK-MB, myoglobin.

Cardiac Enzymes: Troponin

• The most preferred marker for MI since 2004
• High cardiac specificity; released into the blood during an MI.
• Different types of Troponins (Troponin I, Troponin T)
• High sensitivity troponins—Elevated between 4-6 hours post-MI; remain elevated for several days (longer than CK-MB) and peak at 24 hours

Cardiac Enzymes: CK-MB and Myoglobin

• Creatine Kinase (CK) is released when cells die, including elevated CK-MB which is specific for myocardial necrosis.
• CK-MB elevated 4-8 hours post-MI and returns to normal within 2-3 days; peak elevations during first 24 hours.
• Myoglobin: protein released with myocardium injury; elevated 1-4 hours post-injury, good test if patient quickly gets to ER

Diagnosis of Acute MI: Additional Tests

• CXR (chest x-ray): not very specific for MI
• TEE (transesophageal echocardiogram)
• Coronary angiography (angiogram)
• Cardiac catheterization: rules in MI if uncertain; used as a treatment option

Medical Treatment of MIs

• Reduce myocardial oxygen demand
  • Beta blockers, calcium channel blockers
• Increase myocardial oxygen supply
  • Vasodilators (nitroglycerin)
• Improve myocardial muscle function
  • Digitalis glycosides

Surgical Treatment of MIs

• Thrombolysis
• Intra-aortic balloon pump (IABP)
• Percutaneous transluminal coronary angioplasty/percutaneous coronary intervention (PTCA/PCI) with/without stent placement
• Coronary artery bypass graft (CABG)
• Left ventricular assist device (LVAD)
• Cardiac transplantation

NYPH Post-MI Protocol

• Stay within 20-25 bpm of baseline resting heart rate (HR) for first 6-8 weeks post-MI.
• Light warm-up exercises in sitting position.
• Walking program

Cardiac Muscle Pump Dysfunction vs. Failure

• Cardiac muscle dysfunction = small cardiac impairment (decreases in stroke volume [SV], cardiac output, ejection fraction [EF]).
• Cardiac muscle failure = significant decrease in SV, CO, and EF.

Congestive Heart Failure (CHF)

• A syndrome where the heart is unable to pump enough output to meet the body's metabolic demands. It results from any structural or functional cardiac disorder impairing filling of the ventricles or pumping ability.
• Risk factors: CAD, hypertension (HTN), diabetes mellitus (DM), valvular and congenital heart disease, arrhythmias, ethanol/drug abuse and age

Characteristics of CHF

• Dyspnea
• Tachypnea
• Paroxysmal nocturnal dyspnea (PND)
• Orthopnea
• Fatigue
• Peripheral edema
• Cyanosis
• Rales/crackles (especially wet)
• S3 heart sound
• Sinus tachycardia
• Poor exercise tolerance
• Weight gain, hepatomegaly, jugular venous distension (JVD).

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 Function (a review)

• Time for ventricular contraction (ventricular systole)
• 4 major determinants: preload, afterload, contractility, rate of contraction

Diastolic Heart Function (a review)

• Time for filling of the ventricles (ventricular diastole)
• Frank-Starling mechanism: left ventricular end-diastolic pressure (LVEDP) and muscle fiber stretch affect ventricular strength

Systolic Heart Failure

• Decreased contractility leads to pump failure.
• Increased preload leads to pump failure.
• Increased afterload leads to pump failure.
• Changes in chronotropy (heart rate) can also lead to pump failure (too slow or too fast).

Diastolic Heart Failure

• Diastole may be impaired due to excessive hypertrophy of ventricles/composition change of the myocardium
• Reduced end-diastolic volume (EDV): decreased filling of the left ventricle due to increased stiffness in the ventricle wall
• Decreased compliance of the left ventricle leads to increased ventricular pressure.
• Elevated diastolic pressures can lead to reduced cardiac output.

Cardiac/Ventricular Remodeling

• Refers to changes in size, shape, structure, and physiology of the heart after injury to the myocardium. (e.g., MI, chronic hypertension)
• Physiological and pathological changes occur in the zones of infarction, injury, and ischemia.
• Can begin a few minutes after MI and will continue to progress over time.
• Left ventricle changes shape from elliptical to more spherical.
• Apoptosis: programmed death of cells.

Ventricular Remodeling

• Increase ventricular (usually left) size.
• Heart becomes more spherical.
• Functional mitral regurgitation.
• Systolic performance worsens.

Heart Failure (HF) Pathophysiology

• Inability of the heart to provide sufficient output to meet body's demands.
• Multiple disorders can lead to either low or high output failure.
• Pulmonary and systemic venous congestion are common in HF.

Physiological Consequences of CHF

• Cardiovascular: decreased myocardial performance, increased venous return, peripheral vascular constriction, Increased peripheral vascular resistance.
• Neurochemical: increased sympathetic stimulation, desensitization of β1-adrenergic receptors, reduced inotropic effect.
• Pulmonary: development of pulmonary edema due to increased filling pressures.
• Renal: decreased CO, decreased renal blood flow, glomerular filtration rate, sodium & fluid retention, increased arginine vasopressin.
• Musculoskeletal: muscle wasting, skeletal muscle myopathies, osteoporosis.
• Hepatic: possible cardiac cirrhosis, reduced CO.
• Pancreatic: impaired insulin secretion and glucose tolerance.
• Nutritional: anorexia, malnutrition, and cachexia

Summary of Compensation Mechanisms for CHF

• Systems involved:
  • Sympathetic nervous system (SNS)
  • Renin-angiotensin-aldosterone system (RAAS)
  • Natriuretic peptide counter-regulatory system

Compensation for CHF: SNS

• Decreased cardiac output (CO) sensed by baroreceptors leading to increased SNS activity.
• Norepinephrine release to increase HR, myocardial contractility, SV and systemic resistance (vasoconstriction). This increases BP.

Compensation for CHF: RAAS

• Maintains blood pressure (BP) and CO when blood volume depletes.
• Increased venous and atrial tone.
• Increased retention of salt & water.
• Renin release into system to increase Angiotensin II which is a powerful vasoconstrictor.
  • Initially restores BP but possibly leads to decreased CO and decreased renal perfusion.
  • Contributes to remodeling.
  • Promotes release of aldosterone
• Aldosterone is produced in adrenal glands to act on kidneys.

Review of Hormones Involved in CHF

• Norepinephrine
• Renin
• Angiotensinogen
• Aldosterone

Counter-Regulatory Hormones in CHF

• Natriuretic peptides (NPs): ANP, BNP, and c-type NP, stimulated by high ventricular filling pressures
  • Inhibit RAAS
  • Have systemic and renal sympathetic activity
  • Contribute to vasodilation/antihypertensive
  • Increase sodium & water excretion by kidneys
  • Relax the myocardium

Clinical Manifestations of CHF

• Left Ventricular Failure (LVF):

  • Progressive dyspnea (exertion/rest)
  • Dyspnea & orthopnea
  • PND (paroxysmal nocturnal dyspnea)
  • Fatigue/weakness
  • Pulmonary rales
  • S1 heart gallop, S3
  • Enlarged heart
  • Functional MR,TR
  • Signs: Pulmonary edema, pallor, cyanosis, diaphoresis, tachypnea, anxiety, agitation, cerebral hypoxia.

• Right Ventricular Failure (RVF):

  • Dependent edema
  • Hepatomegaly
  • Ascites
  • Fatigue
  • Anorexia, nausea, bloating
  • Right sided S3 or S4
  • Accentuated P2 (closure of pulmonic valve)
  • Pulmonary or Tricuspid valve murmurs
  • Signs: JVD, weight gain, RUQ (liver) pain, jaundice, cyanosis (nail bed), ↓ urine output

Diagnosis of CHF

• Echocardiogram: EF below threshold level (30-40%)
• BNP assay
• Chest X-ray (CXR)
• Electrocardiogram (EKG)
• Hematology/Lab Values: blood values, electrolytes, renal function, liver function
• Cardiac catheterization
• Endomyocardial biopsy

Radiologic Findings of CHF

• Cardiac silhouette
• Edema
  • Interstitial
  • Perivascular
  • Alveolar
• Pleural effusion
• Atelectasis

NYHA Classification of CHF

• Functional Classification: Categorizes patients into four classes based on limitations during physical activity.
• Objective Assessment: Determines presence or absence of objective evidence of cardiovascular disease (Classes A, B, C, D).

Treatment of CHF

• Treatment targets the underlying cause of CHF
• Treatment goals:
  • Improve ability to pump
  • Reduce workload
  • Control sodium intake
  • Control water retention
• Non-drug management
• Medical management
• Surgical management

Non-drug management of CHF

• Cardiac rehabilitation education
  • Understanding signs and symptoms of CHF
  • Importance of taking prescribed medications (including education on how to take medications)
  • Exercise
  • Diet and nutrition (malnutrition, sodium restriction)
  • Fluid restriction, emphasizing the need for it (especially with high-dose diuretics)
  • Importance of daily weighing
  • Alcohol restriction/moderation and smoking cessation

Medical Management of CHF

• Decrease venous return and work of heart
• Increase work of heart
• Diuretics
• Vasodilators (digoxin)
• Beta-blockers
• ACE (angiotensin-converting enzyme) inhibitors
• Inotropes
• Cholesterol-lowering drugs
• Aspirin
• Hemodialysis/ultrafiltration (sometimes)

Surgical Management of CHF

• Cardiac resynchronization therapy (pacemaker)
• Angioplasty with or without stenting
• Athrectomy
• Rotobladder
• Coronary artery bypass grafting (CABG)

Compensated vs. Decompensated CHF

• Compensated CHF: Chronic HF patients on a cocktail of medications with mild/moderate symptoms & a degree of volume overload.
• Decompensated CHF: Baseline abnormalities become further deranged.

Cardiomyopathy (CM)

• Diverse group of diseases involving primary disorders of myocardial cells.
• Disease where contraction, relaxation or both are impaired.
• Secondary causes
• Three main types:
  • Dilated cardiomyopathy (DCM)
  • Hypertrophic cardiomyopathy (HCM)
  • Restrictive cardiomyopathy (RCM)

Dilated Cardiomyopathy (DCM)

• Increased cardiac mass
• Dilatation of all four cardiac chambers.
• Little/no wall thickening
• Systolic dysfunction

Dilated CM (DCM) Results

• Decreased stroke volume
• Impaired ability to increase cardiac output with exercise
• Eventual development of left and right ventricular failure

Hypertrophic Cardiomyopathy (HCM)

• Considerable increase in cardiac mass (hypertrophy)
• No cavity dilatation
• Normal or increased systolic function
• May demonstrate left ventricular outflow obstruction
• Left ventricular hypertrophy causes dysfunction (impairs filling of ventricles)
• Rapid ventricular emptying (may see high EF)
• Often detected during routine medical exam; may hear murmur (S4)

Hypertrophic CM (HCM) Presentation

• First symptom may be sudden collapse/possible death
• Dyspnea and fatigue may occur
• Angina possible (signs)
• Possible syncope/pre-syncope

Restrictive Cardiomyopathy (RCM)

• Rare condition characterized by restriction of ventricular filling.
• Rigid ventricular wall due to loss of compliance.
• Normal or slightly enlarged with dysfunction.
• Causes: Amyloidosis (most common), scarring from unknown causes, heart transplant, carcinoid heart disease, heart tumor, sarcoidosis, scarring post radiation/chemotherapy, others include diseases of the heart lining such as myocardial fibrosis, and scleroderma.

Results in Restrictive CM (RCM)

• Decreased ventricular filling
• Atrial enlargement
• Increased atrial pressures
• Mitral &/or tricuspid regurgitation
• Decreased stroke volume
• Compensatory tachycardia
• Systolic dysfunction may eventually occur

Comparison of Cardiomyopathies

• Illustrates differences in cardiac structure (normal, dilated, hypertrophic, restrictive) for the three primary types of cardiomyopathy

Treatment of CM

• Goals: management of conditions that cause CM, control of signs/symptoms, preventing worsening/complications like death, reducing risk of sudden cardiac arrest.
• Treatment methods are variable, depending on the underlying cause, but may include lifestyle changes, medications (beta blockers, ACE inhibitors, calcium channel blockers, antiarrhythmics, diuretics), surgery (pacemaker, ICD, LVAD, septal myomectomy, transplant), and nonsurgical procedures (alcohol septal ablation).

Valvular Heart Disease

• Normally, heart valves ensure blood flow is one-way through the heart. Each valve has three cusps except for the mitral valve (bicuspid).
• Valves can become stenotic (narrowed), insufficient (leaky), or prolapsed (bulging).
• Signs of exhaustion and heart failure may be present in patients with valvular heart disease.

Causes of Valvular Heart Disease

• Mechanical stress, rheumatic fever, ischemic heart disease, infections, inflammatory diseases, and congenital conditions

Stenosis

• Narrowing or constriction of valves prevents full opening.
• Causes include disease, scars, and abnormal deposits.
• Symptoms include dyspnea and fatigue.

Aortic Stenosis (AS)

• Narrowing of the aortic valve

Mitral Stenosis (MS)

• Narrowing of the mitral valve

Valvular Insufficiency/Regurgitation

• Leaky backflow of blood through valves
• More common on the left side of the heart.
• Valve leaflet abnormalities are also a cause of insufficiency/regurgitation

Aortic Insufficiency (AI)

• Leaky aortic valve

Mitral Regurgitation (MR)

• Leaky mitral valve

Valve Prolapse

• Mostly mitral valve prolapses.
• Leaflets bulge.
• May cause an audible "click."
• Symptoms: fatigue, palpitations, dyspnea, non-anginal chest pain.
• Diagnosis with echocardiogram.

Treating Valve Disease

• Medical Treatments (cannot correct disease, but can reduce workload, regulate rhythms and perhaps slow/halt progression):
  • Medications
• Surgical Treatments (to correct valve disease problems):
  • Commissurotomy, balloon valvotomy, repair (valvuloplasty), valve replacement
  • Mechanical valves; long-lasting, need lifelong anticoagulants. Biological valves do not last as long.

Sudden Cardiac Death

• First clinical manifestation of CAD in ~40% of people.
• Abrupt cessation of heart function: loss of consciousness and arterial pulse.
• Typically results from fatal cardiac arrhythmias (usually due to CAD).
• Common causes: scarring from previous MI, ischemic heart disease, cardiomyopathy, valvular heart disease, electrical abnormalities, blood vessel abnormalities, medications.

Sudden Cardiac Death (Categorization)

• Pulseless VT (ventricular tachycardia)/ V-fib
• Pulseless electrical activity (PEA)
• Asystole
• Outcome depends on early access, CPR, and defibrillation/ACLS.

Aneurysms

• Localized dilatation and weakening of a blood vessel wall that causes pulsating swelling.
• The murmur is a "blowing murmur."
• Could rupture and cause a hemorrhage.
• Thrombosis may form in the pouch and cause emboli that block smaller vessels.
• "Ballooning"
• Dissecting/ Non-dissecting aneurysms
• Types:
  • Saccular
  • Fusiform
  • Mycotic
  • Dissecting

Types of Aneurysms (Continued)

• Mycotic aneurysm: Caused by the growth of fungi or bacteria within the vascular wall (following a septic embolus).
• Dissecting aneurysm: Resulting from hemorrhage (splits arterial wall, creating a tear in the intima, and communication with the lumen).

Aortic Aneurysms

• Infrarenal: Below renal arteries, many located at bifurcation of aorta. May be asymptomatic; if symptomatic it may be due to inflammatory processes. Presents as chronic mid-abd and/or low back pain. Pulsating abd mass may be felt. Rupture may be indicated by severe back/abd pain. 90% of aortic aneurysms.
• Thoracic: Usually due to atherosclerosis, Marfan syndrome, cystic medial necrosis, & vasculitis, or caused by trauma. Usually asymptomatic. Presents with substernal pain, back/neck pain; pressure on trachea or esophagus may cause dyspnea.

Aortic Dissection

• Originates at site of intimal tear & continues distally.
• Proximal dissection
• Distal dissection
• LEATHAL if undiagnosed
  • Usually due to rupture of aorta into pericardial sac or pleural space OR due to acute aortic regurgitation with left ventricular failure.
  • Symptoms often confused with MI or other causes of chest pain.
  • Aggressive measures to lower HTN is usually required prior to surgery.
  • Exceptions: severe pain, rupture of the aorta, ischemia, or progression of the dissection
• Type A vs. Type B
• Often named for locations, ex: AAA, TAA

Peripheral Artery Aneurysms

• Happen mostly in men
• 50% are symptomatic at diagnosis; symptoms come from:
  • Popliteal artery aneurysm: accounts for ~85% of peripheral artery aneurysms
    • Diagnosed and measured by ultrasound.
    • Arteriography defines anatomy of outflow prep before surgery.
  • Femoral artery aneurysm: felt as a pulsatile mass on one or both sides of the thigh; complications are less common compared to popliteal aneurysms. Asymptomatic aneurysms don't typically require surgical treatment; pseudoaneurysms can develop distally at previous aortic surgery sites

Treatment of Aneurysms

• Surgical excision and grafting (endovascular repair [EVAR] vs. open repair)
• Complications include bleeding and MI, respiratory insufficiency, ischemic colitis, limb ischemia, renal insufficiency, and stroke.

Endocarditis

• Inflammation of endocardium (usually microbial infection).
• Typically bacterial infection entering the bloodstream.
• Can cause valve damage.
• Characterized by: Fever, murmur, vegetation, low-grade fever, fatigue, weight loss, night sweats.
• Treatment= antibiotics

Pericarditis

• Inflammation of pericardial sac (pericardium).
• Commonly caused by viral infection but can also be due to cardiac surgery, MI, trauma, tumors, cancer, radiation, autoimmune diseases, or immunosuppressant meds.
• Symptoms: chest pain, dyspnea, high RHR, pericardial rub (on auscultation).
• Possible progression to pericardial effusion (excess fluid).
• May lead to cardiac tamponade (emergency)

Pericarditis Treatment

• Pain relief with positioning (not always effective with MI), aspirin, and NSAIDs.
• Antibiotics for bacterial infection (if that's the cause).
• Surgery if pericardial effusion becomes severe/tamponade risk.
• Pericardiocentesis
• Pericardial window.

Cardiac Tumors

• Generally rare and often curable with surgery.

• Benign tumors (more common)

  • Myxoma - symptoms: DOE, PND, fever, loss of weight, dizziness, syncope, hemoptysis, Raynaud’s, arrhythmias, sudden death.

• Malignant tumors (usually sarcomas)

  • Hemangiosarcomas (common)
  • Rhabdomyosarcomas

• Occasional small benign vascular tumors (i.e. Hemangiomas)

• Cardiac metastases are more frequent than primary neoplasms. Some cardiac tumors have a high propensity for developing pericardial metastases.

• Could be linked with leukemias, melanoma, thyroid cancer, lung cancer, sarcomas, esophageal, renal cell, lymphomas, & breast cancer.


• Tx: treat underlying disease (i.e. Cancer) and/or surgery.

Test your knowledge on heart disease, focusing on coronary artery disease (CAD) and coronary heart disease (CHD). This quiz covers key statistics, risk factors, and pathological processes associated with cardiovascular conditions. Dive deep into the intricacies of heart-related health issues.