[Murmur, contrast, color...? The evaluation of mitral prosthetic regurgitation from the clinical perspective].
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Biomedical subjects
Publications and source records attributed to D García-Dorado.
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Myocardial reperfusion is the single most useful therapeutic approach in patients with acute myocardial infarction. The thousands of lives saved each year by this treatment are the result of scientific progress in very different areas, including the biopathology of myocardial ischemia and reperfusion, the mechanisms of coronary occlusion, the pharmacology of the fibrinolytic system, and clinical research. The 30% reduction in mortality achieved by fibrinolytic treatment in patients with acute myocardial infarction does not fit, apparently, with the short time-window during which restoration of blood flow results in significant myocardial salvage in animal models with few collaterals. This discrepancy could be due to the protective effect of intermittent coronary occlusions immediately preceding stable occlusive thrombosis (ischemic preconditioning), or to other possible beneficial effects of reperfusion independent of myocardial salvage, as limitation of ventricular remodelling or reduction of the risk of cardiac rupture or severe arrhythmias. Clearly, the best approach to increase the beneficial effects of reperfusion therapy is to perform it as early as possible; the cost-effectiveness of pre-hospital treatment strategies is now under investigation. In the other hand, current reperfusion therapy cannot be considered optimal. Thrombolytic agents fail to achieve recanalization of the infarct related vessel in 20-30% of patients, and 10-15% of the successfully opened arteries present early reocclusion. In certain subgroups of patients, such in those with cardiogenic shock, failure rate is higher. Mechanical recanalization by "direct" angioplasty represent an alternative reperfusion method, which utility has been established in certain circumstances only. So, well in the "reperfusion era", many questions remain open.(ABSTRACT TRUNCATED AT 250 WORDS)
The patency of the infarct-related coronary artery seems to be an important prognostic factor after an acute myocardial infarction. It is not only related to short term prognosis, specially in the context of cardiogenic shock, but also to long-term prognosis, due to its influence on ventricular remodelling. On the other hand, the assessment of new fibrinolytic treatments require large numbers of patients in multicenter trials for documenting a benefit, when mortality is used as the endpoint. Accordingly, new endpoints will have to be developed, as the patency of the infarct-related coronary artery. Coronary angiography has been used until now to assess coronary patency. However, it is an invasive procedure and its optimal timing after fibrinolytic treatment has not been established. The classic non-invasive methods, like resolution of chest pain, reperfusion arrhythmias, normalization of ST segment elevation and enzymatic determinations, are not very useful, although the combined analysis of these markers increases their accuracy. The imaging methods, specially isotopic but also magnetic resonance imaging, offer interesting possibilities, but they are expensive and not universally available. The usefulness of contrast echocardiography has not been well established. Thus, the diagnosis of myocardial reperfusion by a non-invasive method, sensitive, specific and with a good temporal and spatial resolution, is still an unsolved problem.
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Histological sections performed 24 h after coronary occlusion in eight pigs displayed compact infarcts extending transmurally with well-defined edges; reconstruction and inspection of the area of necrosis showed a geometric distribution of the infarcts with very irregular, interdigitating edges always in continuity with the main mass of necrosis. Reperfusion in 32 pigs after periods of coronary occlusion of 90, 60, 45, and 30 min exponentially reduced infarct size and transmural extension of the infarct but did not modify its geometry. The two-dimensional size, progression, and geometry of the infarcts could be reproduced by a computer model. In the simulated infarcts, each myocardial cell within the area at risk was represented by a pixel. The algorithm included an inner loop, which determined at random at each iteration a status of reversible or irreversible damage to all pixels. The number of iterations could reproduce infarct of various sizes. With the addition of an index of transmural sensitivity to ischemia, progression of the infarct area could also be reproduced. The only possible means of reproducing the geometry of the infarct was to enter into the program a contiguity condition requiring a direct contact between irreversibly damaged pixels. These observations suggest that the physical interaction between cells is an important determinant of progression of necrosis during coronary occlusion.
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The purpose of this study was to define a model of transient coronary occlusion (CO) in the open-chest pig. The left anterior descending (LAD) coronary artery was occluded at its mid-length in 45 white pigs and reperfusion was performed after 30, 45, 60 or 90 min. One group of 9 animals with permanent CO served as control. During the occlusion period only slight hemodynamic changes were observed, but a period of ventricular arrhythmias was consistently observed between 15 and 30 min after CO, with an incidence of ventricular fibrillation (VF) in 8 cases (18%). All but 1 of the animals with VF could be defibrillated in less than 1 min or 3 electrical countershocks. Complex arrhythmias with marked hypotension were consistently observed after reperfusion. Histological examination showed a patent coronary artery lumen and minor changes in the LAD coronary artery at the site of occlusion in the reperfused animals and completely occluded arteries in the control group. Two pigs (4.4%) died during the night following CO. Transient CO can be performed safely in pigs with a very low complication rate and a high 24-hour survival rate.
A case of acute thrombosis of a mechanical mitral valve prosthesis (Medtronic-Hall) in a 34 weeks pregnant woman is reported. The clinical diagnosis was confirmed by Doppler echocardiography. Emergency surgery was performed starting with a cesarean section to save the fetus, followed by an obstetric hysterectomy. Valve thrombectomy could then be safely carried out. Both, the mother and child could be rescued by this combined intervention and were discharged from the hospital without further complications.
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A high incidence of mitral valve prolapse (MVP) has been reported in various entities which produce important right ventricular (RV) enlargement with normal or decreased left ventricular (LV) volume. To evaluate the importance of RV enlargement in the genesis of MVP in these cases, we analyzed the echocardiographic studies from 176 patients with 'Síndrome Tóxico'. These patients underwent M-mode, cross-sectional and pulsed Doppler examination because of the suspicion of having dietary pulmonary hypertension, a complication which occurred in almost 20% of patients with this epidemic poisoning and which showed a course of gradual resolution in most of them. RV size was classified according to the RV/LV maximal short-axis dimension ratio as normal, border-line, moderately enlarged and severely enlarged. MPV was diagnosed according to standard M-mode and cross-sectional echocardiographic criteria. A second echocardiographic examination was obtained in 38 patients 12.5 +/- 5.3 months after the first one. The incidence of MVP was 9.3% in patients with normal RV size (N = 107), 9.5% in patients with border-line RV size (N = 23), 30% in patients with moderate RV enlargement (N = 30) and 56% in patients with severe RV enlargement (N = 16) (P less than 0.001). Fourteen (77%) of the 18 patients with MVP and moderate or severe RV enlargement (N = 16) (P less than 0.001). Fourteen (77%) of the 18 patients with MVP and moderate or severe RV enlargement had holosystolic MVP. At pulsed Doppler examination, no patient showed signs of mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)
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The role of oxygen free radicals (OFR) generated early during myocardial reperfusion in the genesis of myocardial necrosis was studied in 26 pigs submitted to transient coronary occlusion followed by one of three different reperfusion protocols. In group A, a selective intracoronary infusion of a Ringer solution was started after 60 min of coronary occlusion, and reperfusion was performed 4 min later. The infusion was maintained during the first 6 min of reperfusion at a rate of 3 ml/min. In group B, the Ringer solution administered during reperfusion contained a high concentration (2.778 U/ml) of superoxide dismutase (SOD). In group C, reperfusion was performed after 60 min of coronary occlusion with no intracoronary infusion. Twenty-four hours later the heart was excised and the area at risk and infarct size were measured by in vivo fluorescein injection and triphenyl-tetrazolium chloride staining respectively. The area at risk was similar in the 3 groups: 15.03 +/- 2.6%, 13.26 +/- 3.3% and 16.34 +/- 6.7% of ventricular mass in groups A, B, and C, respectively (p = 0.42). No differences between groups were observed in infarct size, either when measured as a percent of ventricular mass (10.04 +/- 3.8%, 9.31 +/- 3.8% and 10.1 +/- 2.4% in groups A, B, and C, p = 0.91) or as a percent of the area at risk (64.63 +/- 18.5%, 67.81 +/- 16.1%, and 61.35 +/- 6.7%, respectively, p = 0.72). Thus, the intracoronary administration of SOD during the early reperfusion has not beneficial effect on infarct size. This results suggest that the early burst of OFR is not a major determinant of infarct size in the pig.
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