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In the past several decades, cardiovascular pathology has been launched into the forefront of high-quality patient care as a direct result of the virtual explosion in the number and scope of cardiovascular surgical and interventional diagnostic and therapeutic procedures and devices. Cardiovascular pathology informs the practice of cardiovascular surgery and medicine through defining the pathologic anatomy in individual patients and patient cohorts, and in developing and testing procedures and prosthetic devices that facilitate evidence-based choices among surgical or catheter-based interventional options and optimize short- and long-term patient management. Importantly, 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 considerations most relevant to surgery and catheter-based interventions used to diagnose and treat the major forms of acquired cardiovascular disease. It emphasizes pathologic anatomy, clinico-pathologic correlations, and pathophysiologic mechanisms in the various forms of structural heart 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 abbreviated, as they are discussed in greater detail elsewhere in this book. Moreover, although we have not included the key pathologic 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 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 increased size of individual myocytes largely through addition of contractile elements (sarcomeres) and associated cell and tissue elements. 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
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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 ...

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