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Flashcards in Cardiac Pathology 1 Deck (29)
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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



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