Cardiac Pathology 1 Flashcards
Aging of heart - myocardium and chambers
Myocardium and chambers ◦ Decreased LV chamber size
◦ Increased epicardial fat
◦ Myocardial changes:
◦ lipofuscin and basophilic degeneration
◦ Fewer myocytes, increased collagen fibers
Aging of heart - valves
◦ Aortic and mitral valve annular calcification
◦ Fibrous thickening
◦ Mitral valve leaflets buckling towards left atrium → increased left atrium size
◦ Lambl excrescences
Aging of heart - vascular changes
coronary atherosclerosis
Stiffening of the aorta
Congestive heart failure
Occurs when the heart is unable to pump blood at a rate to meet peripheral demand, or can only do so with increased filling pressure.
May result from
◦ Loss of myocardial contractile function (systolic dysfunction)
◦ Loss of ability to fill the ventricles during diastole (diastolic dysfunction)
Cardiac hypertrophy
Cardiac myocytes become hypertrophic when
◦ Sustained pressure or volume overload
◦ Sustained trophic signals (β-adrenergic stimulation)
In the setting of pressure overload
◦ Myocytes become thicker, and the left ventricular wall thickness increases concentrically
In the setting of volume overload
◦ Myocytes elongate, and the ventricular dilation is seen
Hypertrophy of myocytes isn’t accompanied by a matching increase in blood supply
◦ Even though the hypertrophied heart’s energy demands have increased
“the hypertrophied heart is vulnerable to ischemia-related decompensation”
Left-sided heart failure
Can be systolic or diastolic failure
Most commonly a result of ◦ Myocardial ischemia ◦ Hypertension ◦ Left-sided valve disease ◦ Primary myocardial disease
Clinical effects are due to
◦ Congestion in the pulmonary circulation
◦ Decreased tissue perfusion
Left-sided heart failure morphology
Morphologic changes are variable (dependent on the inciting cause)
Left ventricular hypertrophy
Left ventricular dysfunction → left atrial dilation
◦ This can lead to atrial fibrillation, stasis, thrombus
Left-sided heart failure systemic effects
Pulmonary congestion and edema
◦ Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Decreased ejection fraction may result in decreased glomerular perfusion
◦ Stimulating release of renin → increased volume
◦ Prerenal azotemia
Advanced CHF may lead to decreased cerebral perfusion
◦ Hypoxic encephalopathy
Right-sided heart failure
Most common cause is left-sided failure Isolated right-sided failure results from any cause of pulmonary hypertension ◦ Parenchymal lung diseases ◦ Primary pulmonary hypertension ◦ Pulmonary vasoconstriction
Primary right-sided failure
◦ pulmonary congestion is minimal
◦ the venous system is markedly congested
◦ Liver congestion (nutmeg liver)
◦ Splenic congestion → splenomegaly
◦ Effusions involving peritoneal, pleural and pericardial spaces
◦ Edema, especially in dependent areas (e.g., ankles)
◦ Renal congestion
Ischemic heart disease
Results from insufficient perfusion to meet the metabolic demands of the myocardium.
Blood to the myocardium is supplied by the coronary arteries, so any disruption of coronary flow may result in ischemia.
Ischemia may result in ◦ Myocardial infarction ◦ Angina pectoris ◦ Chronic ischemic heart disease, with heart failure ◦ Sudden cardiac death
Secondary to:
Atherosclerosis (>90%)
Chronic vascular occlusion
Acute plaque change - thrombus
Angina pectoris
Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction.
Stable angina
◦ Stenotic occlusion of coronary artery
◦ “squeezing” or burning sensation, relieved by rest or vasodilators
Prinzmetal variant angina
Episodic coronary artery spasm, relieved with vasodilators
Unstable (“crescendo”) angina
◦ Pain, increasing in frequency, duration and severity, eventually at rest ◦ Usually rupture of a plaque, with a partial thrombus
◦ 50% may have evidence of myocardial necrosis
Myocardial infarction - risk factors and causes
Age distribution and risk factors mirror those of atherosclerosis in general, because nearly 90% of infarcts are caused by an atheromatous plaque.
Other causes include:
◦ Embolus
◦ Vasospasm
◦ Ischemia secondary to vasculitis, shock, hematologic abnormalities
Myocardial infarction presentation
◦ Prolonged chest pain (>30 min)
◦ Crushing, stabbing, squeezing, tightness
◦ Radiating down left arm, or to left jaw
◦ Diaphoresis
◦ Dyspnea
◦ Nausea-vomiting
◦ Up to 25% are asymptomatic
Coronary vessels and areas of infarct
LAD (40-50%)
◦ Apex, LV anterior wall, anterior two thirds of septum
RCA (30-40%)
◦ RV free wall, LV posterior wall, posterior third of septum
LCX (15-20%) ◦ LV lateral wall
Evolution of MI
30 min - 4 hr - no gross or micro changes
4-24 hr - dark mottling; coagulation necrosis, eventual PMN involvement
1-3 days - mottling, yellow-tan center; coagulation necrosis, many PMNs
7-10 days - Yellow-tan, soft; phagocytosis of dead cells/debris, granulation tissue
10-14 days - red-gray; granulation tissue, new vessels, early collagen
2-8 wk - gray-white scar; increased collagen
2 mo + - complete scar, dense collagen
Reperfusion
Restoring blood flow to an area of ischemia and impending infarction
◦ An attempt to limit the infarct size by rescuing at risk myocardium
Thrombolysis, angioplasty and stent placement, CABG
Labs most cardiac myocyte-specific
Troponin I and T
Complications of MI - arrhythmia
Half of all MI deaths occur within 1 hour of onset, and are usually secondary to an arrhythmia
Arrhythmia can be a longer-term complication of MI, depending on the site and extent of the lesion
◦ Can result from permanent damage to the conducting system, or from myocardial “irritability” following the infarct
Complications of MI - myocardial rupture
◦ Typically requires a transmural infarct
◦ 2-4 days post MI, when inflammation and necrosis have weakened the wall
◦ Risk factors: ↑ age, large transmural anterior MI, first MI, absence of LV hypertrophy
Complications of MI - infarct expansion
◦ Muscle necrosis → weakening, stretching and thinning of the wall
◦ Mural thrombus often seen
Complications of MI - ventricular aneurysm
◦ Late complication of large transmural infarcts with early expansion ◦ Composed of thinned wall of scarred myocardium
◦ Also associated with mural thrombus
◦ Rupture does not usually occur
Other complications of MI
Contractile dysfunction
◦ Dependent on size of the infarct and associated loss of function
Fibrinous pericarditis
Sudden cardiac death
Unexpected death from cardiac cause, either
◦ Without symptoms, or
◦ Within 1-24 hours of symptom onset
Coronary artery disease precipitates SCD in 80-90%
Other causes include cardiomyopathies, myocarditis, congenital abnormalities of the conduction system, myocardial hypertrophy
Is due to a fatal arrhythmia most often arising from ischemia-induced myocardial irritability
Left-sided hypertensive disease
Pressure overload results in left
ventricular hypertrophy
-The LV wall is concentrically thickened
Diastolic dysfunction can result in left atrial enlargement
-Can lead to atrial fibrillation
May lead to CHF, and is a risk factor for SCD
Right-sided hypertensive disease
Isolated right-sided hypertensive heart disease arises in the setting of pulmonary hypertension.
Acute cor pulmonale may arise from a large pulmonary embolus.
The most common cause of pulmonary hypertension is left-sided heart disease
