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INTRODUCTION

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Cardiovascular pathology defines the morphology and mechanisms of cardiovascular disease in individual patients and patient cohorts, both along the natural history of a disease and following surgery and interventions. The data derived through cardiovascular pathology thereby facilitate evidence-based choices among surgical or catheter-based interventional options and optimize short- and long-term patient management. Beyond implicit clinical benefit for individual patients, the discipline of cardiovascular pathology is a cornerstone of modern cardiovascular research and the preclinical development and clinical implementation of innovative drugs, devices, and other therapeutic options.

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This chapter summarizes pathologic anatomy, clinicopathologic correlations, and pathophysiologic mechanisms in the various forms of structural heart disease most relevant to surgery and catheter-based interventions used to diagnose and treat the major forms of acquired structural cardiovascular disease. In view of space limitations, several important areas (eg, aortic disease) are necessarily omitted from discussion and others (eg, cardiac assist and replacement devices) are focused on details not covered elsewhere in this book. Moreover, although we have not included the key considerations herein, we are mindful that the number of adults with congenital heart disease is increasing rapidly and that they have unique and important clinical and pathologic concerns.1,2

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MYOCARDIAL RESPONSE TO INCREASED WORK AND MYOCARDIAL DISEASE

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Myocardial Hypertrophy

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Hypertrophy is the compensatory response of the cardiac muscle (the myocardium), to increased work (Fig. 5-1).3 This structural and functional adaptation accompanies nearly all forms of heart disease, and its consequences often dominate the clinical picture. Hypertrophy induces an increase in the overall mass and size of the heart that reflects an increased size of individual myocytes largely through addition of contractile elements (the sarcomeres) and associated cell and tissue elements. Substantial and functionally beneficial augmentation of myocyte number (hyperplasia) in response to stress or injury has not been demonstrated in the adult heart.

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FIGURE 5-1

Summary of the gross and microscopic changes in cardiac hypertrophy. (A) Gross photo of heart with hypertrophy caused by aortic stenosis. The wall of the left ventricle is thick and the chamber is not dilated. The left ventricle is on the lower right in this apical four-chamber view of the heart. (B) Altered cardiac configuration in left ventricular hypertrophy without and with dilation, viewed in transverse heart sections. Compared with a normal heart (center of this panel), a pressure overloaded heart, caused for example by aortic valve stenosis (left), has increased mass and a thick left ventricular wall, whereas a volume overloaded heart, caused for example by mitral valve regurgitation, is both hypertrophied and dilated (right), having increased mass with a near normal or diminished wall thickness. (C) Photomicrograph of normal myocardium. (D) Photomicrograph of hypertrophied myocardium at same magnification as (C), showing large cells with enlarged. ([B] Reproduced with permission from Allen HD, Gutgesell HP, Clark EB, et al: ...

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