Myocardial infarction may occur without atherosclerotic lesions discernible by coronary angiography. The impact of this phenomenon may not be appreciated by many clinicians largely because of a priori assumptions that patients who present with a history of MI or angina syndrome are victims of atherosclerosis and fit well into mainstream management ranging from acute care to rehabilitation. In the absence of atherosclerosis, myocardial infarction may result from several etiologies by chronic hypoperfusion if the culprit artery has a course within the myocardium rather than a more epicardial course. These vessels, called tunnelled arteries, are typically traversed by thick bundles of muscle fibres that comprise a myocardial bridge. They are characterized by chronically abnormal hemodynamics that are prone to exacerbation, leading to anginal symptoms and myocardial infarction. A case history is presented that describes the presentation, medical evaluation and treatment, and rehabilitation of a patient with non-atherosclerotic MI attributed to a myocardial bridge. It is followed by a review of the pathophysiology of this medical problem and efficacy of various treatments. Rehabilitation considerations that apply to patients with a tunnelled coronary artery are discussed.

The reduction of myocardial beta-adrenoceptor density in congestive heart failure has been thought to be caused by agonistinduced homologous desensitization. However, recent evidence suggests that excessive adrenergic stimulation may not produce myocardial beta-receptor downregulation unless there is an additional defect in the local norepinephrine (NE) uptake mechanism. To investigate the association between betaadrenoceptor regulation and NE uptake activity, we carried out studies in 30 dogs with right heart failure (RHF) produced by tricuspid avulsion and progressive pulmonary artery constriction and 23 sham-operated control dogs. We determined NE uptake activity by measuring accumulation of IHINE in tissue slices, NE uptake-i carrier density by V3Hlmazindol binding and beta-adrenoceptor density by VHJdihydroalprenolol binding. Compared with sham-operated dogs, RHF dogs showed a 26% decrease in beta-adrenoceptor density, a 51% reduction in NE uptake activity, and a 57% decrease in NE uptake-i carrier density in their right ventricles. In addition, right ventricle beta-receptor density correlated significantly with NE uptake activity and NE uptake-i carrier density. In contrast, neither NE uptake activity nor beta-receptor density in the left ventricle and renal cortex was affected by RHF. Thus, the failing myocardium is associated with an organ-and chamber-specific subnormal neuronal NE uptake. This chamber-specific loss of NE uptake-i carrier could effectively reduce local NE clearance, and represent a local factor that predisposes the failing ventricle to beta-adrenoceptor downregulation.

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