[Isosorbide dinitrate spray: a comparative pharmacodynamic study with a sublingual preparation in patients with chronic cardiac insufficiency].
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Biomedical subjects
Publications and source records attributed to N Marchionni.
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This report describes a case of aneurysm of the ascending aorta with secondary, severe, aortic valve incompetence following temporal arteritis in a sixty-five-year-old woman.
Right cardiac catheterization, serial determination of creatine phosphokinase (CPK) and of CPK-MB activities, and precordial 35-lead ECG mapping were performed in 17 consecutive patients with a first anterior acute myocardial infarction (AMI) within 6 hours of the onset of symptoms. Left ventricular function as determined by the stroke index (SI, ml/m2) to mean pulmonary capillary wedge pressure (PCWP, mmHg) ratio inversely correlated either with the total CPK and CPK-MB released and with peak enzymatic activity, or with the entity of early (6th hour ECG) ST-segment elevation. Conversely, a direct correlation was found between the SI/PCWP ratio and the ratio of R to Q+S waves from late (48th hour) ECG. Residual left ventricular function after a first anterior AMI can therefore be estimated noninvasively in the individual patient by early precordial ECG mapping and by peak enzymatic activity.
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Acute hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate (FDP), an agent that is supposed to restore anaerobic glycolytic flux in the ischemic myocardium, were studied in 40 patients with acute myocardial infarction who were grouped into 4 subsets: subset 1, normal (15 mm Hg or less) pulmonary artery (PA) wedge pressure and normal (35 g-m/m2 or greater) left ventricular (LV) stroke work index; subset 2, elevated (more than 15 mm Hg) PA wedge pressure and normal LV stroke work index; subset 3, normal PA wedge pressure and reduced (less than 35 g-m/m2) LV stroke work index; subset 4, elevated PA wedge pressure and LV stroke work index moderately reduced to a range between 16 and 34 g-m/m2. Patients were randomized into an FDP (250 mg/kg body weight in isotonic saline solution intravenously in 20 minutes) and into a placebo group. Each subset contained 5 FDP- and 5 placebo-treated patients. After basal measurements, hemodynamic measurements were reassessed at 60, 90 and 120 minutes from the infusions, while a standard 12-lead electrocardiogram was recorded in the basal state and 120 minutes after infusion. Nonsignificant hemodynamic change was observed in the placebo subsets, and FDP failed to exert any effect in subsets 1, 2 and 3. A 24% (p less than 0.02) increase in cardiac index occurred 60 minutes after FDP in subset 4. LV stroke work index also increased, while PA wedge pressure remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Hemodynamic effects of digoxin in acute myocardial infarction (AMI) have been acknowledged to depend on the basal cardiocirculatory state. In the present study, the effects of digoxin in patients with AMI were evaluated in four hemodynamic subsets, based on the relationship between mean pulmonary capillary wedge pressure (PCWP, in mm Hg) and left ventricular stroke work index (LVSWI, in g-m/m2): subset 1: normal (less than or equal to 15 mm Hg) PCWP and normal (greater than or equal to 35 g-m/m2) LVSWI; subset 2: elevated (greater than 15 mm Hg) PCWP and normal LVSWI; subset 3: reduced (less than 35 g-m/m2) LVSWI and normal PCWP; and subset 4: elevated PCWP and LVSWI moderately reduced to a range between 16 and 34 g-m/m2. Forty patients were admitted to the study and were randomly assigned to one of two groups in each subset: control group (19 patients) and treated group (21 patients). Five patients were randomized into each of the subsets 2, 3, and 4 in both the control and treated groups, while in subset 1 there were four control and six digoxin-treated patients. Control patients were administered a placebo saline solution and digoxin-treated patients received 0.50 mg of the drug intravenously in 20 minutes. The effects of the placebo and of the drug were evaluated at 30, 60, and 90 minutes from the end of the infusion. Hemodynamic data did not vary in the control group, and digoxin did not exert any relevant effect in subsets 1 and 2. After drug infusion, cardiac index (Cl, in L/min/m2) significantly increased in subset 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
In a series of 75 consecutive patients with transmural acute myocardial infarction (AMI) a right-to-left ventricular filling pressure ratio equal to or greater than 0.65 (RVFP/LVFP greater than or equal to 0.65) was assumed to be indicative of associated right ventricular infarction (RVI). Out of 45 patients with inferoposterior myocardial infarction, 11 (24%) had such hemodynamic evidence of right ventricular infarction (group A). The remaining 34 patients with inferoposterior myocardial infarction (group B) and the 30 patients with anterior myocardial infarction did not. Time-motion and two-dimensional echocardiographic examinations were performed 7-10 days after admission in the 62 patients who survived. Right ventricular wall asynergy was found in six of eight group A patients. In three of these, right ventricular dilatation was also present. No patient in group B with inferior infarction or with anterior infarction showed abnormal right ventricular wall motion. While hemodynamic monitoring seems presently the most specific diagnostic method and it is of invaluable help in the choice of the best pharmacological therapy of right ventricular failure due to RVI, two-dimensional echocardiography is probably highly sensitive and specific for the diagnosis of RVI, by detecting RV wall motion and thickening abnormalities. Due to advantages, such as noninvasivity and repeatibility, two-dimensional echocardiography can be used in the selection of patients who deserve hemodynamic monitoring and in follow-up studies.
In a series of 75 patients with transmural acute myocardial infarction, a right to left ventricular filling pressure ratio equal to or greater than 0.65 was assumed to be indicative of associated right ventricular infarction. Eleven (24%) out of 45 patients with infero-posterior myocardial infarction had such hemodynamic evidence of right ventricular infarction (Group A). The remaining 34 patients with infero-posterior myocardial infarction (Group B) and the 30 patients with anterior myocardial infarction did not. Two-dimentional echocardiographic examination performed 5 days after admission in the 62 patients who survived, showed right ventricular free wall asynergy in six out of eight Group A patients: in three of them right ventricular enlargement was present. No patient in Group B inferior infarction or with anterior myocardial infarction had abnormal right ventricular motion or dimensions.
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A 46-year-old patient showed spontaneous angina with anterior S-T segment depression 30 hours after an inferior acute myocardial infarction. Myocardial ischemia, which was resistant to drug therapy and induced acute left ventricular failure, was promptly reversed by intra-aortic balloon pumping (IABP). Coronary angiography demonstrated diffuse, severe atherosclerotic disease. Efficacy of IABP in this case of spontaneous angina might be ascribed to an increase of the coronary cross-sectional area in response to the increased intraluminal pressure ("passive vasomotion").
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Hemodynamic evaluations of 130 patients with acute myocardial infarction were performed by right and/or left heart catheterization. 115 patients were subdivided in six groups by the pulmonary artery mean pressure (PMP)-left ventricular stroke work index (LVSWI) relationship: 1) normal LVSWI in relation to PMP (14.8% of all cases); 2) increased LVSWI in relation to PMP (0.9%); 3) moderately reduced LVSWI with increased PMP (severe heart failure-cardiogenic shock) (7.0%); 5) reduced LVSWI with low or normal PMP (22.6%); 6) normal LVSWI with elevated PMP (reduced left ventricular compliance or high pulmonary vascular resistance) (15.7%). 28 cases were studied by right and left heart catheterization; in 10 cases only left heart catheterization was performed. Discriminant analysis on the values measured at the first stage of hemodynamic monitoring was conducted: this type of mathematical analysis seemed to provide a more useful prognostic index.
39 patients, subdivided in four groups [I) previous myocardial infarction; II) ischaemic heart disease; III) hypertension; IV) cerebrovascular disease] were administered i.v. low molecular weight dextran in the course of right heart catheterization. The curves of the left ventricular function were determined by the LVSWI-LVFP relationship measured before the test, after the first 150 ml of dextran infusion, at the point of maximal increase of the LVSWI, and at the end of the infusion. The initial values of the LVSWI and SV were lower in the first group with respect to the other three (P less than 0.001), not significantly unlike those of the LVFP. During dextran infusion it is possible to observe an increase of the LVFP in all four groups (P less than 0.01), and of the SV (P less than 0.02) and LVSWI (P less than 0.01 and P less than 0.05, respectively) in the first and the third groups. At the end of the test, different values of the LVSWI (P less than 0.001) and the LVFP (P less than 0.01) were observed in the four groups. The calculated deltaSI/deltaLVFP indices were not significantly different in the four groups, whereas a P less than 0.001 was obtained for the values of the deltaV/deltaLVFP indices (56, 67, 73 and 138 ml/mmHg for the groups I, II, III and IV, respectively). Dextran infusion proved to be a useful test for the hemodynamic assessment of different cardiovascular diseases.
Left ventricular microcatheterization at the bedside was accomplished in 20 acutely ill patients with myocardial infarction. Direct measure of the left ventricular end-diastolic pressure shows that its values can substantially differ from those of the pulmonary artery end-diastolic pressure. The authors observed that left ventricular microcatheterization is indicated, in the course of acute myocardial infarction, in the following circumstances: --when either the pulmonary artery end-diastolic or the pulmonary capillary pressure is beyond normal limits; --in the presence of tachyarrhythmias which, for alteration of the dynamics of atrial contraction, increase the difference between the left ventricular and pulmonary artery end-diastolic pressures; --when a mitralic defect is associated with the acute myocardial infarction.
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