Can be local (compensatory hypertrophy in MI) or global ... Myocardial Stunning: Reversible post-ischemic ... Papillary muscle rupture tends to occur later.
CARDIAC SURGICAL PATHOLOGY
GENERAL CONSIDERATIOS
Myocardial Hypertrophy Compensatory
response of the myocardium to increased work.
Leads
to overall increase in the size and mass of the heart
The
vasculature doesn’t proliferate, leaving hypertrophied myocardium vulnerable to ischemia
MYOCARDIAL HYPERTROPHY
The pattern of hypertrophy reflects the nature of the stimulus.
Concentric Hypertrophy = Pressure overloaded ventricles ( increased mass and thickness without appreciable dilation)
Dilation + Hypertrophy = Volume overloaded ventricles (increased mass, thickness, and chamber radius)
Can be local (compensatory hypertrophy in MI) or global (Valvular heart diseases or dilated CM)
ATHEROSCLEROSIS
Chronic progressive, multifocal disease of vessel wall intima.
The plaque is formed by a process of intimal thickening and lipid accumulation.
Mainly affects large and medium sized muscular arteries
Large epicardial vessels: proximal LAD, Cx, RCA.
THEORY OF ATHEROGENESIS
1st catalyst: Endothelial cell injury Hyperchloestremia Chemicals in cigarettes Viruses Hypertension Hyperglycemia
Functional and phenotypic changes occur in the endothelium, termed endothelial dysfunction.
ENDOTHELIAL DYSFUNCTION
Manifestations: Vasoconstriction
due production of NO
permeability to lipoproteins
Expression Expression
of tissue factor leading to thrombosis
of adhesion molecules leading to adherence of platelets and inflammatory cells.
ATHEROGENESIS
ATHEROGENESIS
Events leading to the formation of a mature plaque Monocyte adherence to endothelial cells and migration to subendothelial space macrophages Smooth muscle cell migration from media to intima and proliferation + secretion of ECM Lipid accumulation, both extracellular and intacellular (foam cells) in both macrophages and SM cells. Lipid oxidation in the vessel walls Persistent chronic inflammation Cell death and release of intracellular lipids
STAGES OF ATHEROSCLEROSIS
NATURAL HISTORY OF ATHEROSCLEROSIS
ISCHEMIC MYOCARDIAL INJURY
Cardiac ischemia occurs when perfusion is inadequate to meet the metabolic demands of the myocardium
The severity and duration of ischemia determine the consequent damage that occurs.
Area at risk: area perfused by obstructed coronary artery. Infarcts extend from the subendocardium towards the epicardium, producing a transmural infarct.
SOME TERMS ASSOCIATED WITH ISCHEMIA
Myocardial Stunning: Reversible post-ischemic myocardial dysfunction.
May occur following CPB, PCI.
Hibernating Myocardium: Viable regions of myocardium with chronically impaired function in the setting of chronically reduced coronary blood flow Myocardial hibernation is characterized by:
Persistent
wall motion abnormality Low myocardial blood flow Evidence of viability of at least some of the affected areas.
HIBERNATING MYOCARDIUM
Contractile function of hibernating myocardium can improve if blood flow returns toward normal or if oxygen demand is reduced (with CABG or PCI)
CAUSES OF CORONARY ARTERY OBSTRUCTION
Fixed Atherosclerotic obstructions (MC)
Autoimmune diseases (SLE, RA)
Vasculitis (Buerger’s disease, Kawasaki)
Coronary artery Spasm (prinzmetal’s)
Dissection
Embolism
Fibromuscular dysplasia
MYOCARDIAL INFARCTION
Coronary plaque rupture with superimposed thrombosis typically lead to a transmural (fullthickness) Q-wave infarct.
Subendocardial infarcts are commonly associated with diffuse stenosing coronary atherosclerosis without acute plaque rupture or superimposed thrombosis in the setting of episodic hypotension, global ischemia, or hypoxemia
FULL THICKNESS VS SUBENDOCARDIAL
MORTALITY AND MORBIDITY
The mortality of AMI has declined from 30% in the 1960s to 10% today.
50% of deaths occur in the 1st hour before the patient reaches the hospital.
Poor prognostic factors: advanced age, female gender, previous MI and DM.
Factors determining long-term prognosis: LV function and extent of obstructing lesions
COMPLICATIONS OF MI Ventricular dysfunction (Myocardial Stunning) Cardiogenic shock (>40% of LV) Arrhythmias (AF, VF, Tachyarrythmias) Myocardial rupture Papillary muscle dysfunction Ventricular aneurysm Pericarditis Systemic arterial embolism (mural thrombi)
COMPLICATIONS OF MI
Mechanical complications tend to occur more in patients with anterior infarcts.
Postero-inferior infarcts tend to have associated conduction abnormalities.
RUPTURE SYNDROMES AND OTHER COMLICATIONS OF MI
CARDIAC RUPTURE SYNDROMES
Rupture of the ventricular free wall (most common).
Rupture of the ventricular septum (less common).
Papillary muscle rupture (least common), resulting in the acute onset of severe MR.
CARDIAC RUPTURE Cardiac rupture is the cause of death in 8- 10% of acute transmural myocardial infarcts. Ruptures tend to occur relatively early following infarction(1st ten days) 25% present within 24 hours of MI. Although the lateral wall is the least common site for left ventricular infarction, it is the most common site for postinfarction free-wall rupture. Rapidly fatal, very rarely amendable by surgery
ACUTE VSD
Complicate 1 to 2% of infarcts.
Without surgery, the prognosis following infarctrelated septal rupture is poor
PAPILLARY MUSCLE DYSFUNCTION
Posteromedial papillary muscle is more susceptible to widespread necrosis and is more commonly (85%) the site of rupture.
Papillary muscle rupture tends to occur later than other rupture syndromes (as late as 1 month after MI).
EFFECTS OF REPERFUSION
Reperfusion occurring before irreversible damage (20 minutes) can limit infarct size or prevent it altogether.
Later reperfusion (6-12hrs) can salvage myocardium located at the leading edge of the wavefront.
CONSEQUENCES OF REPERFUSION
ATHEROSCLEROSIS IN GRAFTS The patency of saphenous vein grafts is reported as 60% at 10 years. Between 1 month and 1 year, graft stenosis is usually caused by intimal hyperplasia with excessive smooth muscle proliferation and extracellular matrix production. Atherosclerosis becomes the more dominant mechanism in graft occlusion beyond 1 to 3 years after CABG.
CAUSES OF ACCELERATED ATHEROSCLEROSIS IN VENOUS GRAFTS Loss of vaso vasorum Nerve damage Acutely increased pressures Medial necrosis Endothelial Damage (during surgical manipulation)
SAPHENOUS VEIN GRAFT ATHEROSCLEROSIS
Atheroembolization is a major risk, often with catastrophic results; due to weakness of the fibrous cap.
LIMA
The IMA has a >90% patency rate at 10 years.
Causes: Minimal
surgical manipulation maintains its nutrient blood supply accustomed to arterial pressures needs no proximal anastomosis, minimal pre-existing ather- osclerosis in most cases.
VALVULAR HEART DISEASE Normal valve function requires structural integrity and coordinated interactions among multiple anatomic components. For the AV valves, these elements include
leaflets, commissures annulus chordae
tendineae papillary muscles
•
For the semilunar valves (aortic and pulmonary), the key structures are the
Cusps Commissures Supporting structures in the aortic and pulmonary roots
PATHOLOGIC DEFINITIONS
Valvular stenosis: defined as inhibition of forward flow secondary to obstruction caused by failure of a valve to open completely.
Valvular insufficiency: defined as reverse flow caused by failure of a valve to close completely.
Both stenosis and insufficiency can coexist in a single valve, usually with one process predominating
AORTIC STENOSIS Prevalence: 2% of the population Etiology: Congenitally abnormal aortic valve (unicuspid or bicuspid) with superimposed calcification. (38%) Degenerative Calcification of trileaflet valve. (33%) Rheumatic heart disease. (24%) Rare causes: Fabry’s disease, SLE, alkaptonuria and Paget’s disease.
AORTIC STENOSIS
PATHOPHYSIOLOGY OF AS
Gradual aortic outflow obstruction due to stenosis
Increased pressure gradient across aortic valve
Concentric LVH to maintain CO
Exhaustion of compensatory mechanisms
Onset of symptoms (angina, syncope) and heart failure
BICUSPID AORTIC VALVE Prevalence: 1% of the population Bicuspid aortic valve (BAV) is the most frequent congenital cardiovascular malformation in humans. Male : Female ratio of 3-4:1. Two cusps are typically of unequal size, Bicuspid valves are predisposed to accelerated calcification, with about 85% becoming stenotic.
Aortic jet velocity, m/sec
Mean gradient, mmHg
Valve area, cm2
Normal
≤1.5
40
