Cardiomyopathy: how far have we come in 25 years, how far yet to go?

Twenty-five years ago clinical investigators began to appreciate that cardiomyopathy is an important and reasonably common form of heart disease. Since then, several functional classifications have been proposed, the specific myocardial diseases have been classified and chronic ischemic ventricular failure has been described. The boundary separating myocarditis from dilated cardiomyopathy remains hazy and, despite intensive research, the causes of dilated cardiomyopathy remain obscure. In particular, we still do not understand the role that may be played by viral infection and alcohol. Myocardial biopsy has proved useful in patients with specific myocardial disorders, heart transplant recipients and patients receiving Adriamycin, but is disappointing in patients with dilated cardiomyopathy. It has become increasingly evident that exercise capacity does not correlate with ventricular function, being highly dependent on peripheral factors. Measurements of oxygen consumption during exercise promise to be useful in assessing treatment of dilated cardiomyopathy. True restrictive cardiomyopathy is uncommon, and the term should be reserved for cardiomyopathies that meet strict criteria. A restrictive component to filling is common to many cardiac disorders, including some cases of cardiac amyloidosis. The concept of hypertrophic cardiomyopathy has evolved rapidly over the past 25 years, and continues to evolve. The importance of arrhythmia as a cause of sudden death is becoming increasingly clear. The place of calcium channel blocking agents in the treatment of hypertrophic cardiomyopathy will probably emerge soon. Amiodarone is finding an increasing role in the treatment of dilated and hypertrophic cardiomyopathy. Surgical treatment is still required for some patients despite unanswered questions on how it works.