[Magnesium in the treatment of acute myocardial infarction. Review and controversies]. / El magnesio en el tratamiento del infarto agudo del miocardio. Revisión y controversias.

The use of magnesium in the current therapeutics of acute myocardial infarction is controversial. There are theoretical bases on possible benefit mechanisms of action, whereby the magnesium have unique properties of myocardial cyto-protection, mainly reperfusion injury. The fundamental aspects about metabolic vias of magnesium, and the pathophysiologic explanations for the beneficial effect of magnesium included prevention of arrhythmia, antiplatelet effect, prevention of reperfusion injury, coronary vasodilation. Deleterious effects are outlined. The results of the main trials have originated considerable discussions in the world cardiology community. The principal differences between these trials and the possible explanations in order to interpret the results are explained.

[The usefulness of determining myoglobin, creatine phosphokinase MB isoenzyme, lactate dehydrogenase and aspartate aminotransferase in the diagnosis of acute myocardial infarct]. / Utilidad de la determinación de mioglobina, isoenzima MB de creatina fosfocinasa, deshidrogenasa láctica y aspartato aminotransferasa, en el diagnóstico de infarto agudo del miocardio.

Diagnosis of acute myocardial infarction is made with the aid of biomarkers such as structural myocardial proteins, myoglobin (MG) or specific enzymes, creatine phosphokinase isoenzyme MB (CK-MB) or non specific enzymes, lactic dehydrogenase (DHL) and aspartate aminotransferase (AST). We found good sensitivity (71%-50%), specificity (85%-100%) and predictive values (Pos. 77%-100%, Neg. 82%-72%) for Mg and CK-MB, supporting their clinical usefulness. In contrast DHL and AST were not clinically useful for early diagnosis.

[Late thrombolysis and electrical stability in acute myocardial infarction. Role of the collateral flow]. / Trombolisis tardía y estabilidad eléctrica en el infarto agudo del miocardio: importancia del flujo colateral.

We evaluated 249 patients (pts) with first acute myocardial infarction: 1. Pts without thrombolysis, n = 119, 2. Pts treated with thrombolysis within 6 hours following MI, n = 80 and 3. Pts treated with thrombolysis between 6-12 hours after MI. Arrhythmic events were evaluated during follow up. All underwent heart rate variability studies and coronary angiogram where anterograde flow (TIMI) and collateral flow (Rentrop scale 0-2 = poor collateral flow and 3 = good collateral flow) were determined. Pts in group 2 and 3 showed a better anterograde and collateral flow than group 1 (p < 0.001). A lower spectral power in the high frequency band and a higher ratio low/high frequency band were observed in group 1 (p < 0.05). Conjunctive consolidation analysis showed more malignant arrhythmias in TIMI 0-2 with poor collateral flow than TIMI 0-2 with good collateral flow (17/138-12.3% vs 0/14-0%). Kaplan Meier analysis was able to demonstrate more cardiac sudden death events in TIMI 0-2 with poor collateral flow than TIMI 0-2 with good collateral flow or TIMI 3 (x2 = 7.22, p = 0.028), independently of thrombolytic treatment.

[Experimental infarction of the right ventricle. Its natural history]. / Infarto experimental del ventrículo derecho. Su historia natural.

To elucidate the pathophysiology of severe right ventricular infarction (RVI), isolated RVI was produced in 12 dogs in an open chest preparation with intact pericardium. After RVI; mean right auricle pressure and right ventricular end-diastolic pressure (RVEDP) increased (p < 0.05). A statistical significant decline was observed in cardiac output (43%, p < 0.05). However, for left ventricular systolic and end diastolic pressures (LVEDP) a decline was noted only after 120, or 90 min of the production of the RVI. Hemodynamic findings suggested a decreased preload of left chambers, as consequence of ischemic injury of the RV. This feature contributes to low cardiac output. A depression in right and left ventricular function curves were noted after RVI and this condition was maintained after 180 min of experimental observation. Equalized end-ventricular diastolic pressures were noted soon after RVI, a finding that was sustained over the time course of the experiment. Equalization of ventricular filling pressures was noted with RVEDP of < than 10 mmHg and with normals LVEDP. This features do not support, as a main cause, a restrictive role of the pericardium in the genesis of equalized filling pressures in RVI.

[Cerebral ischemia secondary to embolism of an aorto-coronary graft. Angiographic findings]. / Isquemia cerebral secundaria a embolia de un injerto aorto-coronario. Evidencia angiográfica.

Ischemic stroke during or following cardiac catheterization may be secondary to diverses mechanisms. Formation and detachment of clots in the catheter wall and embolization of a breaked atheromatous lesion are most frequently. The visualization of clots free in the interior of bypass aortocoronary graft is extremely rare and poorly documented. With angiographic evidence we present a case of cerebral acute ischemia secondary to migration of an embolus from a saphenous vein aortocoronary bypass graft. This case shows a different mechanism of cerebral ischemia.

[The clinical and electrophysiological characteristics of patients with idiopathic ventricular tachycardia]. / Características clínicas y electrofisiológicas en pacientes con taquicardia ventricular idiopática.

Clinical and electrophysiological characteristics in 20 patients with clinical ventricular tachycardia and normal hearts documented by physical examination, echocardiography, and angiocardiography were analysed. There were 11 males and 9 females. All patients had sustained ventricular tachycardia without hemodynamic instability during tachycardia. A right bundle branch block morphology of ventricular tachycardia was present in 14 patients and left bundle branch block morphology in six patients. During electrophysiologic studies, ventricular tachycardia was induced in 10/15 (66%) patients. Intravenous verapamil terminated the ventricular tachycardia in 9/10 (90%) of cases. However oral verapamil not prevented recurrences. Among 14 patients on whom exercise tests were performed, only two had exercise-induced ventricular/tachycardia. Late potentials were positive in 3/14 (21%) cases and one patient died suddenly during exercise without antiarrhythmic drugs.