Search

Ischaemic heart disease is the most common cause of heart failure, but less common causes such as hyperthyroidism should be kept in mind. As a potential reversible cause of cardiomyopathy hyperthyroidism should be excluded in every new patient, young and old, especially in the absence of coronary artery disease. Inspired by an intriguing clinical case we address the question whether hyperthyroidism-related cardiomyopathy is due to tachycardiomyopathy or to thyrotoxic cardiomyopathy.

Experimental observations, made over the past two decades, have led to a profound shift in the conceptual paradigms about the syndrome of heart failure. As a consequence, heart failure is nowadays considered as a complex disease, not merely characterized by haemodynamic disturbances. Instead, it is now believed that the syndrome is governed and impelled by neurohumoral imbalances and by intracardiac paracrine processes. The latter processes are mediated by activated cardiac endothelial cells and by cytokines, creating a state of cardiac maladaption and leading to disease progression. The clinical benefit of several therapeutic interventions that could not be satisfactorily clarified by improvements in the haemodynamic status, may, therefore, be explained by an unexpected impact on cytokines and endothelial dysfunction. Further extension of these insights will form the basis for the future treatment of heart failure.