[The efficacy of isosorbide dinitrate administered in an intravenous bolus in acute cardiogenic pulmonary edema]. / Eficácia do dinitrato de isossorbido administrado em "bólus" intravenoso no edema pulmonar agudo cardiogénico.

STUDY OBJECTIVE: To evaluate the efficacy, safety and tolerability of intravenous (i.v.) isosorbide dinitrate (ISDN) administered as a bolus in the treatment of cardiogenic acute pulmonary edema (CAPE). DESIGN: Clinical, prospective, open, noncontrolled trial. SETTING: Emergency room. PATIENTS AND INTERVENTIONS: Twenty two patients (15 male and 7 female), aged 54 to 80 years (68.4 +/- 6.4) with severe respiratory distress consistent with CAPE were included. The cause of CAPE was chronic ischemic cardiopathy in 13 patients, acute myocardial infarction in four, hypertensive cardiopathy in three and mitral valve disease in two. Patients were excluded from the study because of shock or systolic blood pressure equal or lower than 100 mmHg, severe aortic stenosis, hypertrophic cardiomyopathy and non-cardiogenic pulmonary edema. All patients were placed in the sitting position and received oxygen. Initial therapy consisted of an i.v. bolus of 5 to 10 mg of ISDN. Clinical data were recorded at admission and after 5, 10, 15 and 30 minutes. A new i.v. bolus of ISDN and/or another drug was administered at 5 minutes, when necessary. RESULTS: Fifteen patients treated exclusively with ISDN (in three a second i.v. bolus was necessary) improved markedly. In the remaining seven patients that needed other drugs, the improvement was not so impressive. The mean total dose of i.v. ISDN was 10.34 +/- 3.48 mg. Although all data showed a trend towards improvement, just the following were statistically significant (p < 0.05): pH increased from 7.26 +/- 0.13 to 7.32 +/- 0.9, systolic blood pressure decreased from 192.7 +/- 34.8 mmHg to 155.0 +/- 24.4 mmHg (-19%) and diastolic blood pressure decreased 110.5 +/- 12.7 mmHg to 93.2 +/- 9.1 mmHg (-16%). CONCLUSIONS: In this trial, iv ISDN administered as a bolus in doses ranging from 5 to 20 mg, was effective and safe as a first line agent in the treatment of CAPE. No serious adverse reaction were reported.

[Primary hyperaldosteronism--4 clinical cases]. / Hiperaldosteronismo primário--quatro casos clínicos.

We describe four cases of primary hyperaldosteronism whose initial presentation was a moderate hypertension. Serum potassium and plasmatic aldosterone values were high although plasmatic renin levels were normal. The captopril test (Lyons version), abdominal CT and iodocholesterol (NP-59) scan proved useful to exclude essential hypertension. A good therapeutical results was achieved in all cases by unilateral adrenalectomy. After surgery, diagnosis was confirmed in all cases by histological studies. At one year follow-up, all patients were asymptomatic, with no hypertension without therapeutic and the serum potassium and plasmatic aldosterone and renin values were normal.

[A case of rupture of the free wall of the left ventricle occurring at a district hospital. The problems of communication with heart surgery centers]. / Um caso de rotura da parede livre do ventrículo esquerdo ocorrido em hospital distrital. Problemas de articulação com os centros de cirurgia cardíaca.

This is a report of an acute myocardial infarction complicated with rupture of the free wall of the left ventricle. Some comments concerning diagnosis and therapy are added, with emphasis in the correct communication of community hospitals with the centers of cardiac surgery.

[Fever in the first 48 hours of an acute myocardial infarct treated with fibrinolytics--an indicator of nonreperfusion of the coronary vessels?]. / Febre nas primeiras 48 horas do enfarte agudo do miocárdio tratado com fibrinolíticos--indicador de não reperfusão das coronárias?

UNLABELLED: Fever in the first days of acute myocardial infarction (AMI) is a very common clinical feature, being its prognostic value unquestionable. As infarction area reduction implies a less important fever reaction in the first days of AMI, we believe that thrombolytic therapy would result in a decline of body temperature of patients so treated. That is why we tried to identify such a correlation, and demonstrate the value of normal body temperature as indicative of reperfusion. We studied retrospectively 68 patients (10 F and 58 M, 57.1 +/- 9.6 years) survivors of AMI (I-II KK classes), with (TT) or without (NT) thrombolytic therapy. In NT group, there was an axillary temperature (AX T) higher than 37 degrees C at the first 24 hours in 21 patients (62%); TT group only had 10 patients (30%) with AX T over 37 degrees C (p < 0.01). NT group CK mean peak was 856 +/- 610 U.I./l in patients having AX T > 37 degrees C, and 436 +/- 233 U.I./l when AX T was < or = 37 degrees C (p < 0.05); in TT group there was no difference between CK peak means when AX T was > or < or = 37 degrees C (1508 +/- 1210 U.I./l vs 1406 +/- 1149 U.I./l, respectively) (NA). We established statistic difference between AX T of 15 patients which CK peak was reached after 10 hours over onset of AMI (37.59 +/- 0.36 degrees C) and those (19 p) with CK peak before 10 hours (37.17 +/- 0.60 degrees C) (p < 0.05). NT group presented then more febrile patients than did TT group. CONCLUSIONS: in NT group there was a positive relation between AX T and CK peak level; AX T > 37 degrees C was less frequent in TT group and was as much light when CK peak was more precocious. These results suggest that in thrombolytic treated patients the absence of fever in the first 48 hours may constitute one more coronary reperfusion criterion.

[Effect of intravenous administration of SO4Mg in the acute phase of myocardial infarct]. / Efeito da administração de SO4Mg por via intra-venosa na fase aguda do enfarte do miocárdio.

Fifty four patients (p) with acute myocardial infarction (40M; 14F) were entered into a prospective study where they received either intravenous magnesium sulphate (group A-27 p) or placebo (group B-27 p). The incidence of arrhythmias necessitating treatment was greater in group B (37%) than in group A (15%). Mortality was 18.5% in group B and 3.7% in group A. These results suggest that magnesium sulphate administration reduces the incidence of arrhythmias and death after acute myocardial infarction.

[Therapeutic effectiveness of intravenous magnesium sulfate in tachyarrhythmia. Apropos of 4 clinical cases]. / Eficácia terapêutica do sulfato de magnésio por via intravenosa em taquidisritmias. A propósito de quatro casos clínicos.

This is a report about four patients with tachyarrhythmias successfully treated with intravenous magnesium sulfate. In two cases (supraventricular tachycardia and torsade de pointes) because they were resistant to other antiarrhythmic drugs, and in the remaining two cases (paroxistic atrial fibrillation) because they presented characteristic features of magnesium depletion. The efficacy, the rapid onset of action and the absence of adverse reactions must be emphasized and the authors suggest that larger and randomized trials should be carried out, in order to establish the real place of magnesium sulfate in the antiarrhythmic armamentarium.

Serum and red blood cell Mg levels in acute coronary events.

Serum (s-Mg) and red blood cell (e-Mg) Mg levels were assessed in 29 patients with acute myocardial infarction (AMI) and in 16 patients with unstable angina (UA), from admission until discharge. The following results were found: (1) no significant difference existed between mean s-Mg levels in AMI and UA, despite a tendency for an increase being noted with a favorable course of disease, (2) in AMI, mean s-Mg levels were initially lowered, increased within the first 24 h (p less than 0.05), decreased sharply at day 4 (p less than 0.05), and increased again until discharge (p less than 0.05). (3) in UA; the increase in mean e-Mg during hospitalization is statistically significant (p less than 0.02); (4) no significant difference was found between Mg levels and arrhythmias; and (5) a linear inverse correlation was found between Mg levels and prognosis of infarction.

Serum magnesium levels in patients after myocardial infarction or unstable angina treated with nitrites and calcium antagonists.

A rise of serum Mg levels was observed in patients at 3 and 6 months after acute myocardial infarction, irrespective of therapeutic regimen. In unstable angina follow-up, serum Mg levels remained stable, but below normal values (normal mean values = 2.1 +/- SD 0.4 mg%). A significant difference between mean Mg levels at 6 months was noted in patients with unstable angina treated with calcium antagonists and nitrites as well as in patients treated only with nitrites (p less than 0.02).