Statins competitively inhibit HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis, lowering LDL cholesterol.

Ventricular fibrillation is a shockable rhythm requiring immediate unsynchronized electrical defibrillation as the definitive treatment.

Nitroglycerin causes predominant venodilation, reducing preload and myocardial wall stress/oxygen demand, and also dilates coronary arteries.

Severe symptomatic valvular stenosis (mitral or aortic) typically requires surgical or transcatheter valve replacement/repair for definitive treatment.

Warfarin's anticoagulant effect is monitored via the INR, derived from the prothrombin time (PT).

Antibiotic prophylaxis before certain dental/invasive procedures in high-risk patients (e.g., prosthetic valves) aims to prevent infective endocarditis from transient bacteremia.

Long-term beta-blocker therapy reduces sympathetic overactivation, improving survival and reducing remodeling and arrhythmias in chronic heart failure, despite an initial negative inotropic effect.

ACE inhibitors reduce angiotensin II-mediated vasoconstriction and aldosterone secretion, lowering afterload and limiting adverse ventricular remodeling in heart failure.

New ST-segment elevation in anatomically contiguous ECG leads is the defining finding of STEMI, prompting urgent reperfusion.

Immediate aspirin and prompt reperfusion therapy (primary PCI preferred, or thrombolysis if unavailable in time) are central to acute STEMI management.

Fibrillin-1 defects in Marfan syndrome weaken the aortic wall's elastic tissue, predisposing to aortic root dilation, aneurysm, and dissection.

Eisenmenger syndrome develops when a chronic left-to-right shunt causes pulmonary hypertension severe enough to reverse the shunt direction, producing cyanosis.

Postductal (adult-type) coarctation causes upper extremity hypertension with diminished, delayed femoral pulses (radio-femoral delay).

Patent ductus arteriosus produces a continuous, machinery-like murmur due to persistent flow from aorta to pulmonary artery throughout systole and diastole.

Tetralogy of Fallot consists of a ventricular septal defect, pulmonary (infundibular) stenosis, an overriding aorta, and right ventricular hypertrophy.

Cor pulmonale is right heart strain/failure resulting from pulmonary hypertension due to intrinsic lung disease (e.g., COPD).

Right heart failure leads to systemic venous congestion, causing peripheral edema, hepatomegaly (nutmeg liver), and ascites.

Left-sided heart failure causes pulmonary venous congestion and edema, with alveolar macrophages ingesting extravasated red cells to become hemosiderin-laden "heart failure cells."

Restrictive cardiomyopathy results from stiffening of the ventricular walls by infiltrative processes such as amyloidosis, sarcoidosis, or hemochromatosis, impairing diastolic filling.

Hypertrophic cardiomyopathy typically arises from autosomal dominant mutations in sarcomeric protein genes, causing myocyte disarray and asymmetric septal hypertrophy.

Dilated cardiomyopathy features dilated, thin-walled chambers with impaired systolic contraction, often leading to congestive heart failure.

Libman-Sacks endocarditis is a classic cardiac manifestation of systemic lupus erythematosus.

Marantic endocarditis produces sterile fibrin-platelet vegetations, often associated with malignancy or a hypercoagulable state.

Endocarditis vegetations are friable masses of fibrin, platelets, and microorganisms attached to damaged or abnormal valve surfaces.

In IV drug users, right-sided endocarditis (especially of the tricuspid valve) is characteristic, often due to Staphylococcus aureus.

Aschoff bodies are focal areas of fibrinoid necrosis surrounded by lymphocytes, plasma cells, and characteristic Aschoff giant cells.

The mitral valve is most frequently and severely affected in chronic rheumatic heart disease, often leading to mitral stenosis.

Rheumatic fever follows pharyngitis caused by Group A beta-hemolytic Streptococcus, due to molecular mimicry causing autoimmune damage.

Dressler syndrome is a delayed autoimmune pericarditis occurring weeks to months after myocardial infarction.

Free wall rupture typically occurs 3-7 days after MI, when the infarcted myocardium is maximally weakened by macrophage-mediated debridement before adequate fibrosis.

Fatal ventricular arrhythmias (e.g., ventricular fibrillation) are the most common cause of sudden death in the early hours after MI.

Coagulative necrosis with early neutrophilic infiltration becomes apparent microscopically around 12-24 hours post-infarction.

Cardiac troponins (I and T) are the most sensitive and specific biomarkers for myocardial injury, rising within a few hours and remaining elevated for days.

Fatty streaks, composed of lipid-laden macrophages (foam cells), are the earliest visible atherosclerotic lesions, appearing even in childhood.

Atherosclerotic narrowing of the coronary arteries is the most common cause of ischemic heart disease, including angina and myocardial infarction.

The Bainbridge reflex increases heart rate in response to increased venous return and stretch of the right atrium, mediated via atrial stretch receptors.

During isovolumetric contraction, both sets of valves are closed as ventricular pressure rises without a change in ventricular volume, until it exceeds arterial pressure to open the semilunar valves.

Parasympathetic (vagal) fibers richly innervate the SA and AV nodes, releasing acetylcholine to slow heart rate and AV conduction.

Sympathetic norepinephrine acting on cardiac beta-1 adrenergic receptors increases heart rate (chronotropy) and contractility (inotropy).

MAP is approximately Diastolic Pressure + 1/3(Pulse Pressure), reflecting perfusion pressure over the cardiac cycle.

Arterioles, as the primary resistance vessels, have the greatest influence on total peripheral resistance through changes in their diameter.

The dicrotic notch reflects a brief backflow of blood against the closing aortic valve at the end of ventricular ejection.

Increased heart rate and contractility substantially raise myocardial oxygen consumption, important in ischemic heart disease management.

Increased baroreceptor firing inhibits sympathetic and enhances parasympathetic (vagal) outflow, reducing heart rate and blood pressure back toward normal.

Baroreceptors detect stretch of the vessel wall due to changes in arterial pressure, triggering reflex adjustments in heart rate and vascular tone.

S2 results from closure of the aortic and pulmonic (semilunar) valves at the end of ventricular systole.

S1 is produced by closure of the atrioventricular (mitral and tricuspid) valves at the onset of ventricular systole.

Ejection fraction (EF) = Stroke Volume / End-Diastolic Volume, normally about 55-70%.

Afterload is the resistance/pressure the ventricle must overcome to eject blood into the aorta or pulmonary trunk.

Increased end-diastolic volume (preload) stretches cardiac muscle fibers, increasing the force of contraction and stroke volume, up to a physiological limit.

Cardiac output = Heart Rate x Stroke Volume.

The plateau phase results from a balance between slow inward Ca2+ current (via L-type channels) and outward K+ current.

Phase 0 (rapid depolarization) of the ventricular action potential results from a fast influx of Na+ through voltage-gated sodium channels.

AV nodal delay allows atrial contraction to complete ventricular filling before the ventricles are stimulated to contract.

The SA node normally discharges at 60-100 beats/min, setting the resting heart rate.

Atrial myocytes contain specific secretory granules releasing ANP in response to atrial stretch, promoting natriuresis and diuresis.

Cardiac muscle is striated (like skeletal muscle) but under involuntary autonomic control (like smooth muscle).

Vasa vasorum are small nutrient vessels within the walls of large arteries and veins, supplying the outer tunica media and adventitia.

Venous valves, folds of the tunica intima, are especially numerous in the veins of the lower limbs to counteract gravity.

Discontinuous sinusoidal capillaries with large gaps and incomplete basement membrane are found in liver, spleen, and bone marrow.

Fenestrated capillaries with small pores facilitate rapid exchange, found in kidney glomeruli, intestinal villi, and endocrine glands.

Continuous capillaries, common in muscle, skin, and the CNS, have a complete basement membrane and tight junctions, restricting permeability.

Muscular (distributing) arteries have a tunica media rich in smooth muscle, allowing regulation of vessel diameter and blood flow.

The aorta and its major branches are elastic arteries, with abundant elastin in the tunica media to accommodate pulsatile flow.

Purkinje fibers are larger than typical cardiomyocytes, contain abundant glycogen, and have fewer peripheral myofibrils, allowing rapid impulse conduction.

The AV node lies in the lower interatrial septum, near the opening of the coronary sinus.

The SA node lies in the right atrial wall near the entrance of the superior vena cava.

Gap junctions permit ions to pass directly between adjacent cardiomyocytes, enabling the heart to function as an electrical syncytium.

Cardiac myocytes have intercalated discs (containing gap junctions and desmosomes) and typically one, occasionally two, centrally located nuclei.

The endocardium, composed of endothelium and subendothelial connective tissue, lines the heart's inner surface and valves.

Endocardial cushions contribute to septation of the atrioventricular canal, forming parts of the atrial and ventricular septa and the AV valves.

The ductus venosus allows oxygenated umbilical vein blood to largely bypass the hepatic sinusoids, draining into the IVC.

Anterosuperior displacement of the infundibular septum produces the four features of Tetralogy of Fallot: VSD, overriding aorta, pulmonary stenosis, and RV hypertrophy.

The right horn of the sinus venosus is incorporated into the right atrium, forming its smooth-walled portion (sinus venarum).

Cardiac neural crest cells migrate to contribute to the aorticopulmonary septum and outflow tract (conotruncal) cushions; their disruption is linked to conotruncal defects like Tetralogy of Fallot.

Coarctation of the aorta typically occurs near the site of ductus arteriosus attachment, either preductal (infantile) or postductal (adult) type.

The proximal right subclavian artery arises from the right 4th aortic arch (plus the right dorsal aorta distally).

The distal part of the left 6th aortic arch persists as the ductus arteriosus, connecting the pulmonary trunk to the aorta in the fetus.

Incomplete division of the truncus arteriosus by the aorticopulmonary septum results in a single common arterial outflow vessel (persistent truncus arteriosus).

The membranous interventricular septum forms from tissue derived from the endocardial cushions, fusing with the muscular septum below.

Failure of the septum primum and secundum to fuse/seal after birth leaves a patent foramen ovale, a type of atrial septal defect.

The septum primum and septum secundum together (with overlap forming the foramen ovale) create the interatrial septum.

The primitive ventricle forms the bulk of the definitive left ventricle, with the bulbus cordis contributing to the right ventricle.

The primitive heart tube begins rhythmic contractions and pumping around the 22nd-24th day (~week 4).

The heart develops mainly from splanchnic mesoderm of the cardiogenic (primary heart) field, with later contributions from the second heart field and neural crest.

The azygos vein arches over the root of the right lung to drain into the superior vena cava.

The great cardiac vein accompanies the LAD artery in the anterior interventricular groove.

The ligamentum arteriosum connects the pulmonary trunk (or left pulmonary artery) to the arch of the aorta.

The tricuspid valve, with three cusps, guards the opening between the right atrium and right ventricle.

The mitral valve, with two cusps, lies between the left atrium and left ventricle.

The vagus nerve provides parasympathetic innervation to the heart, notably slowing SA/AV nodal conduction.

The transverse sinus is a passage behind the aorta and pulmonary trunk, anterior to the atria, surgically useful for clamping great vessels.

Excess fluid/blood in the pericardial cavity restricts cardiac filling, producing tamponade.

The fibrous pericardium blends inferiorly with the central tendon of the diaphragm, anchoring the heart.

The LAD is one of the two main terminal branches of the left coronary artery, supplying the anterior interventricular septum and anterior left ventricle.

In about 90% of people (right dominant circulation), the SA node is supplied by the right coronary artery.

The coronary sinus lies in the posterior atrioventricular groove and drains into the right atrium.

The apex, formed by the left ventricle, is normally palpable in the 5th left intercostal space at the midclavicular line.

The right atrium forms the right heart border on a standard chest radiograph.

The heart and pericardium occupy the middle mediastinum, between the two pleural cavities.