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Biomedical subjects

G Morgano

Publications and source records attributed to G Morgano.

At least 37 records · Page 2Linked to original sources
PubMed1988

Diastolic function in acute myocardial infarction: a radionuclide study.

We studied left ventricular diastolic function by equilibrium gated radionuclide angiography in patients as follows: 75 with acute myocardial infarction (AMI), 35 with anterior or anteroseptal necrosis (Group A) and 40 with inferior, inferolateral, or posterior necrosis (Group I). The ejection fraction (EF) was lower in Group A than Group I (41.9 +/- 2.5 vs. 57.1 +/- 2.0%, p less than 0.001), as was peak diastolic filling rate normalized to end diastolic volume (PDFR-EDV/sec) (1.9 +/- 0.1 vs. 2.4 +/- 0.1 EDV/sec, p less than 0.05). PDFR normalized to stroke volume was similar in both groups. An excellent linear correlation was found between EF and PDFR-EDV/sec in the total study population. Isovolumic relaxation period (IRP) was beyond our upper normal value of 94 msec in 64% of patients and it was shorter in Group A than I (95.8 +/- 12.7 vs. 147.0 +/- 13.6 msec, p less than 0.05). The presence of shorter IRP in Group A than in I is probably a result of an earlier mitral valve opening as a consequence of higher left atrial pressure.

Adult↗
PubMed1988

[Different modalities of classification and prognostic significance of ventricular arrhythmias after acute myocardial infarct. Prospective study].

In our study we compared the prognostic significance of clinical variables, laboratory results and different classification models of ventricular ectopic beats recorded by means of a pre-discharge 24 hour ambulatory electrocardiographic monitoring, in 210 survivors of acute myocardial infarction. In addition a full multivariate analysis of the factors affecting survival time was carried out using Cox's proportional hazards (multiple) regression model. Multivariate stepwise discriminant analysis identified hypertension, congestive heart failure assessed by Killip class, and the grading system for ventricular arrhythmias as the most important prognostic variables. When Moss grading system for ventricular arrhythmias was used, the relative risk was a superior as heavy Moss grading system (Moss 2 vs Moss 1 and Moss 3-4 vs Moss 1, relative risk = 1.2 and 3.6 total death, respectively). Furthermore, the hazard ratio of Moss grading system was higher utilizing as comparison patients without ventricular ectopic beats (relative risk = 1.7 for Moss 2 and 5.3 for Moss 3-4) than patients with ventricular ectopic beats less than one/hour (relative risk = 1.2 for Moss 2 and 3.7 for Moss 3-4). Thus, in survivors of acute myocardial infarction, a rational and useful ventricular ectopic beats categorization includes both frequency and the presence or absence of malignant characteristics.

Adult↗
PubMed1986

Effect of nifedipine on dipyridamole thallium-201 myocardial scintigraphy.

The effect of a calcium antagonist drug, nifedipine, on dipyridamole thallium-201 images was assessed in 10 angina patients with positive dipyridamole test. Two dipyridamole thallium-201 tests were performed, the first in basal conditions, the second after administration of 20 mg nifedipine. After dipyridamole, heart rate and double product increased respectively from 68.0 +/- 8.2 to 94.7 +/- 11.5 beats/min (p less than 0.01) and from 9459.5 +/- 1800.2 to 12,770.0 +/- 1864.7 mmHg X beats/min (p less than 0.01). Dipyridamole when infused after nifedipine induced an increase in heart rate from 74.2 +/- 7.16 to 88.8 +/- 5.6 beats/min (p less than 0.01) and in double product from 9650.5 +/- 1348.0 to 11,399.0 +/- 1146 mmHg X beats/min (p less than 0.05). Systolic and diastolic blood pressures were unmodified during the two studies. Segment scores were comparable before and after nifedipine. Thus, nifedipine does not worsen thallium-201 myocardial images obtained during dipyridamole infusion, therefore, this test could provide an alternative to exercise thallium-201 in patients receiving calcium antagonist drugs.

Coronary Circulation↗
PubMed1986

Two-dimensional echocardiographic evaluation of ventricular asynergy induced by dipyridamole: correlation with thallium scanning.

Myocardial asynergies detected by two-dimensional echocardiography during intravenous administration of Dipyridamole (0.75 mg/kg) were evaluated in 54 patients referred for angiographic evaluation of chest pain. Technically adequate two-dimensional echocardiograms suitable for analysis were recorded in 42 of 54 (77.7%) patients studied. Thallium-201 myocardial perfusion scintigraphy, during dipyridamole test was performed in the same patients. Thirty of the 42 patients studied showed significant coronary narrowing at cardiac catheterization. Dipyridamole-induced wall motion abnormalities and myocardial perfusion defects were detected, respectively, in 19 (63.3%) and 21 (70%) of 30 patients with significant coronary artery disease. Wall by wall comparison of the distribution of dipyridamole-induced echocardiographic asynergy with reversible thallium-201 (201Tl) perfusion defects demonstrated complete correlation in 42 segments examined. Three segments with perfusion defects at thallium scanning did not show asynergy during the test while two segments showing wall motion abnormalities during dipyridamole infusion did not manifest perfusion defects. Our study demonstrates that two-dimensional echocardiography during dipyridamole testing is useful in detecting patients with coronary artery disease. Furthermore, ventricular asynergies detected during the test show a high correspondence with site of myocardial perfusion defects at thallium scanning.

Cardiac Catheterization↗
PubMed1986

[Involvement and function of the right ventricle in acute myocardial infarct. Hemodynamic, echocardiographic and angioscintigraphic correlations].

To assess the acute effects of myocardial infarction on right ventricular function 22 patients were studied utilizing right heart catheterization, radionuclide angiography and two dimensional echocardiography. Thirteen patients had inferior myocardial infarction (Group I) and 9 anteroseptal or anterior (Group II). Hemodynamic findings suggesting right ventricular infarction were present in 3 patients of Group I. Mean radionuclide right ventricular ejection fraction was lower in inferior myocardial patients (38.2 +/- 7.6-Group I vs 50.3 +/- 11.4-Group II, p less than 0.005), while left ventricular ejection fraction in anteroseptal, and anterior myocardial infarction patients (36.8 +/- 10.5-Group II vs 55.9 +/- 7.6-Group I, p less than 0.001). Six patients in Group I presented a depressed radionuclide right ventricular ejection fraction (less than 40%): moreover right ventricular ejection fraction correlated with left ventricular ejection fraction in Group II (r = 0.79, p less than 0.001) but not in Group I (r = 0.55, p = NS). By mean of 2 dimensional echocardiography Group I patients had an increased right ventricular end diastolic area (15.3 +/- 3.8 vs 12.1 +/- 1.2 cm2, p less than 0.05) while Group II an increased right ventricular free wall motion (47.3 +/- 10.7 vs 32.4 +/- 14.1%, p less than 0.005); right ventricular end diastolic area correlated with right ventricular ejection fraction only in Group I (r = 0.60, p less than 0.05). Five patients in Group I and no patients in Group II had an enlarged right ventricular end diastolic area. Therefore, radionuclide and echocardiographic evidence of right ventricular involvement were not always associated with abnormal hemodynamics. Thus, the damaged right ventricular chamber dilates to allow an adequate stroke volume in presence of low ejection fraction; hemodynamic significant right ventricular myocardial infarction becomes evident only in patients with more severe right ventricular compromise; the increase in right ventricular free wall motion in anterior myocardial infarction patients compensates the loss of contribution of interventricular septum contraction.

Adult↗
PubMed1986

Effect of mexiletine on reperfusion-induced ventricular arrhythmias: comparison with lidocaine.

Thirty mongrel dogs underwent proximal occlusion of the left anterior descending coronary artery to evaluate the comparative action of mexiletine and lidocaine on ventricular arrhythmias during myocardial reperfusion. Heart rate, arterial blood pressure, left ventricular end-diastolic pressure and dp/dt max were evaluated before and at the 20th and 25th min after coronary occlusion; at the 25th min coronary occlusion was removed. Dogs were randomly assigned to one of the following groups of 10: 1) control group; 2) dogs given i.v. mexiletine; 3) dogs given i.v. lidocaine. As expected, during ischemia, myocardial contractility decreased after mexiletine or lidocaine administration more than in the control group. Ventricular arrhythmias during myocardial reperfusion occurred in 9 dogs of the control group (ventricular tachycardia in 2 cases and ventricular fibrillation in 7 cases). Among dogs given mexiletine only 1 had ventricular fibrillation (p less than 0.001 vs control). Six of the 10 dogs given lidocaine had ventricular arrhythmias (ventricular tachycardia in 5 cases and ventricular fibrillation in 1 case) (p = ns vs control group; p less than 0.05 vs mexiletine group). Thus mexiletine and lidocaine had similar effects on cardiac function during myocardial ischemia and only mexiletine showed a protective effect against reperfusion ventricular arrhythmias.

Animals↗
PubMed1984

Effect of beta-blockade on thallium-201 dipyridamole myocardial scintigraphy.

The effect of beta-blockade on dipyridamole thallium-201 images was assessed in 8 patients with coronary artery disease and positive dipyridamole test. Three dipyridamole thallium-201 tests were performed, the first in basal conditions, the second 30' after propranolol and the third with propranolol and atrial pacing. After dipyridamole heart rate and double product increased respectively from 75 +/- 7 to 98 +/- 15 b/min (p less than 0.01 vs starting values) and from 10 551 +/- 1255 to 11 740 +/- 4542 mmHg X b/min (p less than 0.05 vs starting values). Propranolol reduced heart rate to 64 +/- 6 b/min (p less than 0.05 vs basal conditions), systolic blood pressure to 136 +/- 13 and double product to 8733 +/- 1248 (p less than 0.05 vs basal conditions). Dipyridamole when infused after propranolol, induced an increase in heart rate to 70 +/- 5 b/min (p less than 0.05 vs starting values) while double product was 9133 +/- 1189 mmHg X b/min (p = NS vs starting values). Atrial pacing prevented the fall in heart rate and double product induced by propranolol so during dipyridamole infusion double product increased to 13 271 +/- 1868 (p less than 0.05 vs propranolol treatment; p less than 0.05 vs starting values). Segmental score calculated after dipyridamole was 5.2 +/- 2.0 in basal conditions, 5.1 +/- 1.3 after propranolol (p = NS) and 4.8 +/- 1.3 after propranolol plus atrial pacing (p = NS). Thus the results of the study show that beta-blockade does not worsen dipyridamole thallium-201 images. Furthermore the steal phenomenon seems to be the main mechanism of the dipyridamole induced ischemia. In fact, also when the increase, oxygen consumption is blunted with beta-blockade the disparity in myocardial blood flow resulted unaffected.

Blood Pressure↗