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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Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

Subarachnoid hemorrhage (SAH) is a devastating condition. It carries a high mortality rate, with 12% of patients dying before reaching the hospital. Aside from its neurological morbidities, SAH is associated with significant medical complications. Cardiac manifestations are common and can impact morbidity and mortality in SAH patients. This article will discuss the cardiac manifestations of SAH.

Background. The reductions of myocardial 83-adrenergic receptor density and responsiveness to catecholamines in congestive heart failure are associated with excessive sympathetic stimulation. The purpose of this study was to determine whether the myocardial changes could be prevented by /3-receptor blockade.Methods and Results. We administered the oral /3-receptor blocking agent nadolol (40 mg/day) to dogs during an early stage of experimental right heart failure and to sham-operated dogs for 5 weeks. Animals receiving no nadolol were studied concurrently. Nadolol treatment did not prevent right ventricular hypertrophy or elevated concentrations of plasma norepinephrine that occurred in right heart failure, nor did it affect the decrease in myocardial norepinephrine content and norepinephrine uptake activity, suggesting that the hemodynamic stress imposed on the right ventricle of dogs with right heart failure was similar regardless of the presence or absence of /3-receptor blockade. Resting heart rate, right atrial pressure, aortic pressure, cardiac output, right ventricular dP/dt, and left ventricular dP/dt and dP/dt/P measured 5 days after discontinuation of nadolol did not differ significantly from those without nadolol treatment in either right heart failure or sham-operated animals. Sham-operated dogs also showed no changes in myocardial /3-receptor or adenylate cyclase activity after nadolol treatment. However, nadolol treatment prevented the reduction of myocardial /3-receptor density and attenuated the decrease in the cardiac /3-adrenergic sensitivity that occurred in right heart failure.Conclusions. Excessive sympathetic stimulation may play an important role in the development of /-receptor downregulation and /-adrenergic subsensitivity in right heart failure. (Circulation 1991;84:254-266)

Percutaneous closure of a secundum atrial septal defect was performed successfully via the jugular approach in a 77-year-old patient with heparin-induced thrombocytopenia and total occlusion of the inferior vena cava using the Amplatzer septal occluder after an unsuccessful attempt using the CardioSEAL septal occluder. This case demonstrates the advantages of the jugular approach in the patient with difficult anatomy and the advantage of the Amplatzer over the CardioSEAL device in this situation.

Very late stent thrombosis is a feared complication after drug-eluting stent (DES) implantation. Several factors related to the patient, generation and type of the deployed stent, procedure, and premature antiplatelet withdrawal are known to contribute to this complication. Herein, we describe a case of a Jehovah's witness patient who developed simultaneous two-vessel 1st generation DES thrombosis 5.4 and 3.5 years after deployment [with sparing of the bare metal stent (BMS)] in the immediate postoperative period secondary to clopidogrel withdrawal. The case was complicated by ST-segment elevation myocardial infarction, cardiogenic shock, and a ventricular fibrillation cardiac arrest requiring urgent percutaneous coronary intervention. The acute thrombosis of DESs with sparing of the BMS exemplify how they are more prone to this complication due to delayed endothelialization of stent struts and neoinitimal coverage.