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      Coronary Sclerosis, Myocardial Infarction, Myocarditis, Cardiomyopathy, Coronary Anomalies, and the Cardiac Conduction System

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      Springer Berlin Heidelberg

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          Isolation of a common receptor for Coxsackie B viruses and adenoviruses 2 and 5.

          A complementary DNA clone has been isolated that encodes a coxsackievirus and adenovirus receptor (CAR). When transfected with CAR complementary DNA, nonpermissive hamster cells became susceptible to coxsackie B virus attachment and infection. Furthermore, consistent with previous studies demonstrating that adenovirus infection depends on attachment of a viral fiber to the target cell, CAR-transfected hamster cells bound adenovirus in a fiber-dependent fashion and showed a 100-fold increase in susceptibility to virus-mediated gene transfer. Identification of CAR as a receptor for these two unrelated and structurally distinct viral pathogens is important for understanding viral pathogenesis and has implications for therapeutic gene delivery with adenovirus vectors.
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            Coronary artery anomalies in 126,595 patients undergoing coronary arteriography.

            Coronary artery anomalies were found in 1,686 patients (1.3% incidence) undergoing coronary arteriography at the Cleveland Clinic Foundation from 1960 to 1988. Of the 1,686 patients, 1,461 (87%) had anomalies of origin and distribution, and 225 (13%) had coronary artery fistulae. Most coronary anomalies did not result in signs, symptoms, or complications, and usually were discovered as incidental findings at the time of catheterization. Eighty-one percent were "benign" anomalies: 1) separate origin of the left anterior descending and circumflex from the left sinus of Valsalva; 2) ectopic origin of the circumflex from the right sinus of Valsalva; 3) ectopic coronary origin from the posterior sinus of Valsalva; 4) anomalous coronary origin from the ascending aorta; 5) absent circumflex; 6) intercoronary communications; and 7) small coronary artery fistulae. Other anomalies may be associated with potentially serious sequelae such as angina pectoris, myocardial infarction, syncope, cardiac arrhythmias, congestive heart failure, or sudden death. Potentially serious anomalies include: 1) ectopic coronary origin from the pulmonary artery; 2) ectopic coronary origin from the opposite aortic sinus; 3) single coronary artery; and 4) large coronary fistulae. Coronary artery anomalies require accurate recognition, and at times, surgical correction.
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              Isolated noncompaction of left ventricular myocardium. A study of eight cases.

              Isolated noncompaction of left ventricular myocardium is a rare disorder of endomyocardial morphogenesis characterized by numerous, excessively prominent ventricular trabeculations and deep intertrabecular recesses. This study comprised eight cases, including three at necropsy. Ages ranged from 11 months to 22.5 years, with follow-up as long as 5 years. Gross morphological severity ranged from moderately abnormal ventricular trabeculations to profoundly abnormal, loosely compacted trabeculations. Echocardiographic images were diagnostic and corresponded to the morphological appearances at necropsy. The depths of the intertrabecular recesses were assessed by a quantitative echocardiographic X-to-Y ratio and were significantly greater than in normal control subjects (p less than 0.001). Clinical manifestations of the disorder included depressed left ventricular systolic function in five patients, ventricular arrhythmias in five, systemic embolization in three, distinctive facial dysmorphism in three, and familial recurrence in four patients. We conclude that isolated noncompaction of left ventricular myocardium is a rare if not unique disorder with characteristic morphological features that can be identified by two-dimensional echocardiography. The incidence of cardiovascular complications is high. The disorder may be associated with facial dysmorphism and familial recurrence.
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                Book Chapter
                2011
                August 3 2011
                : 241-282
                10.1007/978-3-642-20659-7_13
                49c47758-e9cc-48c8-a310-43d83406e622
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