HEART WEIGHT Total heart weight is the most reliable single measurement at autopsy for correlation with cardiac disease states (7). The assessment must take into account the size of the patient. Other described measurements such as linear external dimensions, surface areas, and volume of the entire heart or myocardium (7) are less useful than the total heart weight.
Hearts are weighed after the parietal pericardium has been removed, the great vessels have been trimmed to about 2 cm in length, and postmortem clots have been removed from the cardiac chambers. Weights are recorded to the nearest gram (3,6) (or at least to the nearest 5 g in adults). For subjects younger than 1 yr, scales should be used that weigh accurately to the nearest 0.1 g. Fixation may alter heart weight by 5-10% (31, 32). Among the numerous available tables of normal values (5-7,32-34) the variation has generally been less than 10%.
Normal expected heart weights are related to age, gender, and body size (32-34) (see also Part III of this book). Normal heart weight usually correlates better with body weight than with age or height (33,34). In some settings, for instance if patients received massive fluid therapy for shock or had a recent amputation, expected heart weight should be based on height or on the body weight before fluid therapy or amputation.
CARDIAC WALL THICKNESS Left ventricular thickness has usually been measured 1-2 cm below the mitral annulus (5), but because wall thickness is greatest at the base and least at the apex, the most reliable average measurement is found at the level of the papillary muscles. The ventricular septum and the right ventricle should be measured at the same level. All three values can readily be attained from hearts dissected by the short-axis method. Trabeculations and papillary muscles should not be included in the measurements. Fixation may increase left ventricular wall thickness by 10% (31). Right ventricular thickness is usually greater inferiorly than anteriorly. Normal values should only be compared to nondilated hearts (see Part III of this book) (31,33,34).
With the rare exception of stone heart (intractable systolic contracture), the heart at death stops in asystole, not systole or diastole. Initially, the heart is flaccid (7) but within an hour, it begins to develop rigor mortis. Therefore, the left ventricular wall thickness and chamber dimensions generally resemble those in end-systole (35). About 24 h after death, rigor mortis remits, left ventricular wall thickness decreases again, and the chambers dilate, a condition not to be confused with dilated cardiomyopathy.
CARDIAC CHAMBER SIZES After death, chamber sizes may change considerably because of rigor mortis (see above) or fixation (which decreases ventricular volumes by about 50%) or because of perfusion fixation (which may increase them appreciably) (36). This makes the interpretation of chamber volumes difficult. From the internal long-axis length (L) and short-axis diameter (D), a formula (nLD2/6) may be used to calculate left ventricular volume.
CARDIAC HYPERTROPHY AND DILATATION For nondilated hearts from adults who show rigor mortis, hypertrophy is generally present if left ventricular wall thickness exceeds 1.5 cm or if right ventricular wall thickness exceeds 0.5 cm (7). For dilated hearts, however, these measurements are not reliable. Thus, total heart weight is the best gross indicator of cardiac hypertrophy, when compared to expected normal weight (see p. 568 in Part III of this book) (37). For research studies, the partition method is recommended, with comparison to tables of normal values for each chamber (6,7,20).
There is no gross or microscopic difference between physiologic hypertrophy of athletes and pathologic hypertrophy that results from disease states (6). However, in athletes, the heart weight is rarely increased more than 25% above the expected value. Ischemic heart disease alone, without coexistent hypertension, generally produces only mild hypertrophy, affecting all four chambers, and a heart weight of <550 g (38).
In chronic disorders such as systemic hypertension, aortic stenosis, dilated or hypertrophic cardiomyopathy, and congenital heart disease, the heart often weighs 2.0-2.5 times the expected value, or about 600-900 g in adults. Weights exceeding 1000 g may be found in hypertrophic cardiomyopathy, chronic aortic regurgitation, and acromegaly with hypertension. Isolated right ventricular hypertrophy due to pulmonary hypertension rarely produces a heart weight above 500 g.
Volume hypertrophy (avoid the potentially misleading term, eccentric hypertrophy ) of the left ventricle is always accompanied by chamber dilatation and secondary wall thinning. In hearts from adults of average size with rigor mortis, the short-axis internal dimension of the left ventricle is normally <2.5 cm. This measurement can be used to estimate the severity of left ventricular dilatation (see p. 570 in Part III of this book). The wall thickness of a dilated left ventricle cannot be used as an accurate indicator of hypertrophy (37,39); instead, the overall heart weight is used for this purpose. The other three cardiac chambers are normally thin-walled; thus, hypertrophy and dilatation are not as readily quantitated as for the left ventricle, and pressure hypertrophy is often attended by substantial dilatation. All dilated chambers should be evaluated for mural thrombi, particularly within atrial appendages, ventricular apices, and ventricular aneurysms.
CARDIAC VALVE SIZE Valve function is difficult to evaluate at autopsy (6). Regurgitation can be assessed to some extent by filling the chambers with water to check for retrograde flow through the intact valve. Stenosis is best evaluated by measuring the effective orifice size.
For intact hearts, valve diameters can be measured with a ruler or a calibrated cone (Fig. 3-9A) (32). A cone will distort the elliptical orifices of the mitral and tricuspid valves, producing minor inaccuracies. In stenotic valves, cones measure orifice size rather than annular size.
Most pathologists measure valve circumferences (rather than diameters) along the annulus of the atrioventricular valves and at the arterial sinotubular junction of the semilunar valves. Measurements should be to the nearest 0.1 cm. Standard fixation may decrease valvular circumferences by 10-25% (31), whereas perfusion fixation generally increases the measurements, particularly for the right-sided valves. For a given body size, women have slightly larger valves than men (34).Valve circumferences, particularly those of the semilunar valves, progressively dilate during adult life (34,40). The thickness and area of leaflets and cusps also increase with age. For normal values and their interpretation, and for further references, see Part III of this book (32-34,40).
PATENCY OF THE FORAMEN OVALE Postnatally, the foramen ovale closes either anatomically or only functionally,
as a flap-valve. A patent foramen ovale may later serve as an avenue of paradoxical embolization and, therefore, its presence should be recorded. If an interatrial passageway is present, a probe can be passed from the right atrium between the valve and limb of the fossa ovalis, or from the left atrium from the ostium secundum. The maximum potential diameter of the foramen ovale is best established using graduated probes (Fig. 3-9B). For normal values (41), see Part III of this book.
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