Peaks of QTc lengthening measured in Holter recordings as a marker of life-threatening arrhythmias in postmyocardial infarction patients.
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Biomedical subjects
Publications and source records attributed to V Martí.
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BACKGROUND: Detection and treatment for rejection after transplantation are based on the identification of myocyte damage upon endomyocardial biopsy. Noninvasive detection of such damage is possible with 111In-labeled monoclonal antimyosin antibodies (MAA). Although the presence and degree of MAA uptake parallels the rejection activity detected by biopsy, the relation between the degree of uptake and the occurrence of severe rejection-related complications has not been previously assessed. METHODS AND RESULTS: Two hundred forty-seven MAA studies were performed coinciding with biopsies in 52 patients 1-71 months after transplantation. A heart-to-lung ratio (HLR) was used as a measure of relative MAA uptake, with an HLR of 1.55 discriminating normal from abnormal studies. Of the 247 antimyosin studies, 149 coincided with absent, 38 with mild, and 60 with moderate rejection at biopsy. HLR was 1.68 +/- 0.27, 1.79 +/- 0.22, and 1.91 +/- 0.33 in the three biopsy groups, respectively (p less than 0.0001). Two hundred thirty-eight of 247 antimyosin studies coexisted with absent rejection-related complications; in nine of 247 patients, such complications were detected (five congestive heart failure episodes due to rejection and four episodes of vascular occlusion, which resulted in five deaths), and mean HLR was 1.74 +/- 0.3 and 2.1 +/- 0.16 in the two groups, respectively (p less than 0.0001). No complications were noted in 193 studies of patients with HLR of less than 2.00, whereas in nine of 45 with HRL of 2.00 or greater, complications occurred (p less than 0.0001). None of the 23 patients prospectively followed since surgery who had a gradual decrease in MAA uptake during the first 3 months showed rejection-related complications, whereas persistent uptake was associated with complications in five of nine patients (p less than 0.001). CONCLUSIONS: No rejection-related complications are seen coinciding with HLR of less than 2.00, whereas patients who have complications have an HLR of more than 2.00. The early 3-month pattern of decreasing MAA uptake is associated with a clinical course free of rejection-related complications, whereas a persistent pattern is a signal of the possibility of such complications.
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Dysfunction of a prosthesis implanted in tricuspid position is a severe complication that may develop with minimal symptoms. A patient who presented clinical manifestations of heart failure for two weeks due to obstruction of a mechanical prosthesis in tricuspid position is described. Fibrinolytic treatment was given unsuccessfully, therefore prosthetic replacement was performed. In the removed prosthesis, a fibrotic pannus which developed in the strut and disc was seen. We review the clinical manifestations, the diagnosis and treatment of the dysfunction of a prosthesis implanted in tricuspid position.
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In a 4-year interval, 3/55 (7.8%) heart transplant recipients developed (greater than 4 weeks) severe sinus node dysfunction. An epicardial ventricular pacemaker was implanted at 90, 40, and 38 days after operation. Follow-up ranged from 7 to 20 months. In two of the three cases, failure of stimulation or sensing was detected at the 3rd and 4th month after pacemaker implantation. Sinus rhythm reappeared in two of the three patients at the 2nd and 4th months after transplantation. Severe sinus node disease requiring pacemaker implantation can improve following the first 3 months after transplantation. Failure of stimulation or sensing may not be uncommon.
We analyze retrospectively the short- and long-term results of coronary artery bypass surgery in 50 patients with severe left ventricular dysfunction operated in a period of 11 years. Sixty-six percent of patients had unstable angina and 12% of total presented angina post-acute postmyocardial infarction. Thirty-eight percent of patients were in preoperative functional class III-IV of NYHA. Three-vessel disease was present in 70% of the patients, two-vessel in 30%, and the main trunk was affected in 12% of the global. Hospital mortality was 4% (2/50) due to low cardiac output syndrome. Follow-up was available in all the survivors and ranged 6 months-11 years (mean: 4.8 +/- 3.1). During follow-up, 13 patients died, but in only six was due to cardiac cause. The 35 patients followed were in functional class I-II of NYHA. Eighty-eight percent of the patients were angina free at follow-up. Actuarial analysis, after exclusion of 3 patients who died of causes no directly related to the heart, showed an intrahospital survival rates of 96%; at first year was 92, at 3rd was 78%, and 5th year survival rates were 75%. In conclusion, patients with symptomatic angina and preoperative severe left ventricular dysfunction, coronary artery bypass graft has a low hospital mortality, is effective in improving angina and heart failure, and the long-term survival is acceptable.
Ninety-six coronary angiographies of 30 orthotopic heart transplant recipients were studied. Eleven coronary artery fistulas to right ventricle were seen in 7 (23.3%) patients; five involved the left anterior descending artery, four the right coronary artery, and two the circumflex artery. All the coronary arterial fistulas appeared within the first year after transplantation, when endomyocardial biopsies were more frequent. In the review of the histologic samples, we found coronary arterioles greater than 0.15 mm of diameter in 3 of 7 patients with coronary arterial fistula; on the contrary, those were not found in any of the 69 histologic samples of 23 heart transplant patients without coronary fistula (p less than 0.001). Neither clinic nor hemodynamic abnormalities were seen in any patient during the follow-up. The coronary fistula had a benign course, with a tendency to decrease in size and to close spontaneously.
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A 32-year-old man with Hodgkin's disease presented an acute myocardial infarction following mediastinal irradiation. A complete occlusion at the level of the proximal segment of the right coronary artery and a moderate stenosis of the left circumflex coronary artery was demonstrated by selective coronary angiography. An inferior hypokinesia was seen by the ventricular angiography. We discuss the possible role of the mediastinal irradiation in the induction of coronary heart disease as well as the importance of an early diagnosis.
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A 7 months-old child affected of West syndrome presented a cardiac hypertrophy with subaortic obstruction induced by adrenocorticotropic hormone treatment. The administration of this hormone may induce a Cushing syndrome; at high doses has chronotropic and inotropic positive effects and may produce arterial hypertension and cardiac hypertrophy. We pointed out the importance of the echocardiography-Doppler in the diagnosis and follow-up of the cardiac hypertrophy with subaortic obstruction as well as the reversibility of the cardiac involvement when the drug is suppressed.
A retrospective study was undertaken of 31 patients submitted to tricuspid valve replacement between 1977 and 1988, either alone or associated to mitral or aortic replacement. The cause of the tricuspid lesion was rheumatic in 19 patients, congenital in seven, prosthetic valve thrombosis in two and miscellaneous in the remaining 3 patients (endocarditis, carcinoid syndrome, iatrogenic operative tricuspid regurgitation). Of the 31 tricuspid prostheses reviewed, 26 were mechanical (St Jude, Björk-Shiley) and five of the biological type (Ionescu, Hancock). Results showed that 25% of patients died in the hospital; 75% of them had been operated previously. With a follow-up averaging 3.9 years the complications related with the prosthesis were: thrombosis of the tricuspid prostheses in 1 patient (1.2% patients-year) and hemolytic anemia in another. Ninety percent of patient included in the follow-up were in NYHA class I or II. Three patients (14%) died due to a cause not directly related to the prosthesis. An actuarial analysis showed intrahospital survival rates of 55%, 100% and 75% in patient with 3, 2 and 1 prostheses, respectively; at 6 months postoperatively the figures were 55%, 87% and 75%, and at a follow-up of 3 years, 55%, 67% and 66%. In conclusion, in patients submitted to a tricuspid valve replacement mortality is high before hospital discharge, and is related to the clinical situation. A sustained improvement is observed in survivors once discharged, independently of the number of prostheses implanted. Complications related to the tricuspid prosthesis are comparable to those observed with prostheses in mitral or aortic position.
A patient with a single coronary artery originating in the right coronary sinus is presented. The condition was diagnosed during aortic valve replacement surgery and later confirmed by coronary angiogram. The clinic significance in relation to the anomalous course of the coronary artery and the importance of correct diagnosis prior to cardiac surgery is discussed.
We studied 16 patients with electrocardiographic evidence of advanced interatrial block and retrograde activation of the left atrium (P greater than or equal to 0.12 s, and diphasic (+/-) P waves in leads II, III, and VF). Eight patients had valvular heart disease, four had dilated cardiomyopathy and four had other forms of heart disease. Patients with valvular heart disease and cardiomyopathy were compared with a control group of 22 patients with similar clinical and echocardiographic characteristics, but without this type of interatrial block. Patients with advanced interatrial block and retrograde activation of the left atrium had a much higher incidence of paroxysmal supraventricular tachyarrhythmias (93.7%) during follow-up than did the control group, (27.7%) (P less than 0.001). Eleven of 16 patients (68.7%) with advanced interatrial block and retrograde activation of left atrium had atrial flutter (atypical in seven cases, typical in two cases, and with two or more morphologies in two cases). Six patients from the control group (27.7%) had sustained atrial tachyarrhythmias (five atrial fibrillation and one typical atrial flutter). The atrial tachyarrhythmias were due more to advanced interatrial block and retrograde activation of left atrium and frequent atrial extrasystoles than to left atrial enlargement, because the control group with a left atrium of the same size, but without advanced interatrial block and retrograde activation of left atrium and with less incidence of atrial extrasystoles, had a much lower incidence of paroxysmal tachycardia.
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