Sirolimus and tacrolimus in clinical cardiac transplantation.
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Biomedical subjects
Publications and source records attributed to S M Mallon.
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Cerebral phaeohyphomycosis is a rare disease caused by dematiaceous (darkly pigmented) fungi. Cladophialophora species are highly neurotropic, and Cladophialophora bantiana (synonym=Xylohypha bantiana or C. trichoides) is the most commonly identified agent. Most reported cases of cerebral phaeohyphomycosis have occurred in immunocompetent patients; however, some case reports and experimental data have suggested that cellular immune deficiency is a risk factor. We report a case of pulmonary and cerebral phaeohyphomycosis in a cardiac transplant patient due to a newly identified species of Cladophialophora. Optimal management includes both antifungal therapy and surgery.
The efficacy of holmium laser-assisted angioplasty was studied in 365 narrowings in 331 consecutive patients with coronary artery disease. Clinical indications for study were unstable angina pectoris in 140 patients (42%), stable angina in 136 patients (41%), postmyocardial infarction angina in 35 patients (10.5%), silent myocardial ischemia in 11 patients (3%), acute myocardial infarction in 1 patient (0.3%) and undefined in 8 patients (2%). Coronary morphology characteristics by Multivessel Angioplasty Prognosis Study group criteria were type A in 12.6%, type B1 in 34.2%, type B2 in 27.4% and type C in 25.4%. The laser successfully crossed the total length of the narrowing in 85.2%. Procedural success was 94.2%. Laser alone reduced mean percent luminal narrowing from 88 +/- 11% to 57 +/- 22%. Subsequent balloon angioplasty further reduced the mean luminal narrowing to 23 +/- 18%. Major complication rate was 2.7% (death 0.3%, Q-wave myocardial infarction 0.5%, and emergent bypass surgery 2.7%). Six-month angiographic restenosis (> 50% stenosis) rate was 44%.
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BACKGROUND: Silent myocardial ischemia in patients with coronary atherosclerosis is associated with an increased risk of adverse cardiac events, including sudden death. The relation between silent ischemia and the initiation of potentially fatal ventricular arrhythmias has not been defined, however. METHODS: As part of a long-term study of sudden cardiac death, data on arrhythmias, coronary anatomy, and responses to ergonovine testing to provoke coronary-artery spasm were collected prospectively among survivors of out-of-hospital cardiac arrest who had no flow-limiting coronary-artery lesions, prior myocardial infarctions, or other structural causes of cardiac arrest and no angina pectoris. Associations between silent myocardial ischemia due to coronary-artery spasm and the occurrence and characteristics of life-threatening ventricular arrhythmias were studied by both invasive and noninvasive techniques. RESULTS: Silent ischemic events were associated with the initiation of life-threatening ventricular arrhythmias in five patients with induced or spontaneous focal coronary-artery spasm (or both). These patients were identified among a group of 356 survivors of out-of-hospital cardiac arrest who were evaluated between 1980 and 1991. In two of the five patients reperfusion, rather than ischemia itself, correlated with the onset of the ventricular arrhythmia. Only one of the five had an inducible arrhythmia during electrophysiologic testing. Titration of the dose of a calcium-entry-blocking agent (verapamil, diltiazem, or nifedipine) against the ability of ergonovine to provoke spasm was successful in preventing both the provocation of spasm and arrhythmias in all four patients who were tested. CONCLUSIONS: Silent myocardial ischemia due to coronary-artery spasm can initiate potentially fatal arrhythmias in patients without flow-limiting structural coronary-artery lesions. The role of silent ischemia, reperfusion, or both in the initiation of fatal arrhythmias in larger groups of patients with advanced coronary-artery lesions remains to be defined.
Among 13010 adults who underwent coronary arteriography, 80 (0.61%) patients had a total of 83 anomalous coronary arteries. Thirty-three (41%) of the patients were of Hispanic origin, while out of the entire population studied 30% were Hispanic. The right coronary artery was the most common anomalous vessel. It was identified in 50 (62%) patients, arising in 35 from the left aortic sinus, in 14 from the posterior sinus, and in 1 from the left coronary artery. An anomalous circumflex artery was recognized in 22 (27%) patients. Nine (11%) patients presented an anomalous left anterior descending artery, 1 patient an anomalous left main coronary artery, and another an anomalous septal perforator artery. Twenty-three (29%) patients had concomitant congenital heart abnormalities, most commonly. bicuspid aortic valve and mitral valve prolapse. In each of 5 patients with complex congenital heart disease the course of the anomalous vessel could have interfered with a surgical procedure. In 4 cases anomalous coronary arteries were associated with either anomalous systemic venous circulation or anomalous cardiac veins. In 5 (6%) patients only, the anomalous coronary artery was solely responsible for a clinical event. Coronary atherosclerosis of the anomalous arteries was found in 28% of the patients, while the overall incidence of the disease in this series was 65%. Thus, anomalous coronary arteries are associated with a high incidence of congenital heart diseases, but do not appear to be associated with an increased risk for development of coronary atherosclerosis. The angiographic recognition of these vessels is important in patients who undergo coronary angioplasty or cardiac surgery. Variations in the frequency of congenital coronary anomalies as reported herein may be attributed to a genetic background.
Spontaneous coronary artery dissection is a rare event and only in a few patients has the diagnosis been angiographically confirmed during life. A spontaneous dissection of the right coronary artery was detected as a cause of out-of-hospital cardiac arrest in a patient with coronary artery ectasia.
Twenty-two young adult (mean age 27.8 +/- 5.3 years) survivors of sudden cardiac arrest underwent invasive cardiac assessment. Initial evaluation by cardiac catheterization, coronary angiography, and hemodynamic studies identified two groups of young survivors. The first consisted of 13 (60%) subjects who had definable structural cardiac or lung disease accountable for a cardiac arrest event. Dilated cardiomyopathy dominated this group. Mitral valve prolapse, hypertrophic cardiomyopathy, left ventricular hypertrophy, anomalous origin of the right coronary artery, and tetralogy of Fallot were also encountered. The second group included nine subjects (40%) with normal cardiac structure and normal hemodynamic parameters. Electrophysiologic testing demonstrated in three of these patients the presence of Wolff-Parkinson-White syndrome. The electrophysiologic studies had a higher yield in reproduction of life-threatening arrhythmias among the subjects in the second group as opposed to the first group. The observation that 10 subjects (45%) from both groups had preceding symptoms varying from palpitations and chest pain to syncope and recurrent cardiac arrest events, is in contradiction to previous findings in the literature and raises a question of appropriate evaluation of young adults with cardiac symptoms.
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Twenty patients with acute ventricular septal rupture underwent cardiac catheterization. Prior to catheterization, 17 patients were in Killip class 3-4. Mean cardiac index and cardiac output were 2.03 +/- 0.81 L/min/m2 and 3.55 +/- 1.33 L/min, respectively. Based on a recent pathologic description of septal rupture, we encountered by angiography and during surgery, two morphologic types of rupture: simple type which appears as a direct through-and-through communication between the ventricles, and complex type which presents hemorrhagic tracts in the septum with the opening into the ventricles at different levels. Considering the management of patients with septal rupture and the clinical outcome in our series, it is suggested that there is a need to minimize invasive angiographic procedures prior to early surgical correction of the ruptured septum.
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The long-term survival following valve replacement with Carpentier-Edwards or Hancock bioprostheses was compared between the two valve models and between the two groups totaling 407 patients who were discharged after valve replacement beginning in 1974. The two groups of patients were treated in a nonrandomized fashion. The actuarial survival for 299 patients with Carpentier-Edwards valves was 94 +/- 1.5% (+/- standard error) and 93 +/- 1.7% after 5 and 8 years of follow-up, respectively. Comparable figures for 108 patients undergoing valve replacement with Hancock valves were 89 +/- 3.0% and 83 +/- 3.7%, respectively (p = not significant [NS]). The probability of freedom from death and valve removal after 5 and 8 years of follow-up was 91 +/- 1.8% and 79 +/- 4.6%, respectively, with the Carpentier-Edwards valve and 84 +/- 3.5% and 75 +/- 4.3%, respectively, with the Hancock valve (p = NS). An accelerated rate of attrition for both valves was observed in the mitral position. There were no significant differences in actuarial survival between the two valves in the mitral or the aortic position or in the incidence of major valve-related complications.
Three children were identified as having anomalous origin of the left anterior descending coronary artery (LAD) from the pulmonary artery (PA). Two had had congestive heart failure in infancy with clinical diagnosis of endocardial fibroelastosis and all had abnormal ECGs. The correct diagnosis was delayed in each case, and two patients required selective coronary angiography. Surgery was accomplished in the three children although ECG abnormalities have persisted and one child has dyskinesis of the left ventricular apex. Because this diagnosis may be difficult to make when intercoronary anastomoses are inadequate to outline the left anterior descending coronary flow into the PA, patients with clinical findings suggestive of anomalous coronary artery may require selective coronary studies to exclude this anomaly.
To assess the efficacy of a new calcium entry blocker, diltiazem (Cardizem), for prophylaxis of Prinzmetal's angina, 48 patients were studied in randomized, multiple crossover multiclinic study (2 weeks single-blind, 8 weeks double-blind). Diltiazem dosage in one crossover phase was 120 mg per day; in the other, 240 mg per day. Therapeutic response was measured by patients' diary records of angina frequency and nitroglycerin tablet consumption. Treatment with 120 mg of diltiazem per day reduced angina by 41 percent from the entry placebo period and 20 percent from the paired placebo period (p less than 0.005). Treatment with 240 mg of diltiazem per day reduced angina frequency by 68 percent from the entry placebo period and 43 percent from the paired placebo period (p less than 0.01). There were similar reductions in nitroglycerin consumption. Adverse experiences that may have been related to the medication were noted in only 5 percent of patients. There were no alterations in blood pressure or heart rate. The PR interval increased 3 percent at the 240 mg dosage level. We conclude that diltiazem is an effective and safe agent for control of symptoms of Prinzmetal's angina.
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The effect of the addition of radiographic contrast material (Renografin) to blood on the oxyhemoglobin dissociation curve and P50 was measured by a metabolic deoxygenation technique in a strongly buffered red cell suspension. With incubation time constant, increasing doses produced progressive decreases in P50. With incubation time varied at a constant dose, a decrease in P50 was seen after only one minute. In addition, in vivo studies were performed on 11 patients undergoing cardiac catheterization. Simultaneous proximal coronary sinus and aortic samples were drawn as controls, and then at one minute and five minutes after injection of the left coronary artery. In eight patients studies were performed after, and in three prior to left ventriculography. At one minute after left coronary injection there was a significant decrease of coronary sinus as compared to aortic P50 (p less than .10) (only when left ventriculography was performed prior to coronary arteriography). The magnitude of these effects in vivo is unknown, but they would be expected to be more severe in areas distal to a critical coronary lesion due to stasis of blood flow and ischemic metabolic changes.