Search PubMed⌕ Search

Biomedical subjects

J Salerno

Publications and source records attributed to J Salerno.

At least 37 records · Page 2Linked to original sources

[Effects of medical and surgical therapy on the long-term survival of patients with variant angina].

To determine the effects on survival of the medical and surgical treatment of variant angina, we compared the prognosis of 75 surgically treated subjects with that of 75 medically treated patients, selected from a series of 340 consecutive patients observed between January 1969 and December 1982. The patients were selected on the basis of a developed computer program to match each medically treated patient with one surgically treated patient so that each pair was similar according to the following clinical and angiographic variables: sex, age, previous myocardial infarction, severe ventricular arrhythmias during pain, site of ST elevation (anterior or inferior), coronary artery disease (single or multivessel), left ventricular function (normal or abnormal). Patients who were considered unoperable because of poor ventricular function or distal vessel disease were not included in this study. Mantel-Haenszel log-rank analysis demonstrated a significantly better prognosis in surgically treated patients, particularly in those with multivessel disease as well as in those with ST elevation in anterior leads. However survival in 63 medical patients who were treated with calcium-antagonists was not significantly different from that of their surgical matched patients. During the follow-up period, anginal symptoms were more frequently found in medically treated patients (p less than 0.05). We conclude that in patients with variant angina surgical treatment does not improve survival as compared to medical treatment with calcium blocking drugs. Coronary artery bypass surgery can be carried out at low risk and is particularly indicated in those patients with angina refractory to medical treatment.

Angina Pectoris, Variant↗

Ventricular septal rupture after myocardial infarction: diagnosis by two-dimensional and pulsed Doppler echocardiography.

Rupture of the ventricular septum in the acute phase of myocardial infarction (MI) requires prompt recognition for correct management. The 2-dimensional and pulsed Doppler echocardiographic findings are reported from 11 patients with ventricular septal (VS) rupture. VS rupture was confirmed by cardiac catheterization in 9 patients, surgery in 4 patients and necropsy examination in 3 patients. Two-dimensional echocardiography (echo) directly visualized the rupture in 7 patients and assessed the size and location of an associated aneurysm in 10. In all patients, M-mode pulsed Doppler echo allowed detection of the left-to-right shunting due to VS rupture, but failed to indicate the rupture site. M-mode pulsed Doppler echo was reliable for detecting VS rupture after MI. Conversely, 2-dimensional echo was less effective in the direct visualization of the rupture, but provided anatomic and functional information that was useful in medical and surgical management. Thus, the techniques are complementary and should be used in combination for the assessment of VS rupture in acute MI.

Adult↗

Variable threshold exertional angina in patients with transient vasospastic myocardial ischemia. Repeat exercise test results and therapeutic implications.

Thirty-five of 70 patients with vasospastic angina at rest complained of chest pain during exercise or during usual daily activity. In 22, the angina threshold was described as variable during exercise: that is, the amount of exertion that induced angina was not always the same. In 12 patients with variable threshold exertional angina, 3 exercise tests performed in the morning on different days yielded different results, because chest pain and ischemic electrocardiographic changes occurred at different work loads with a wide range in heart rate-systolic pressure product. Two patients, in whom great cardiac vein flow was measured during exercise before and after taking nifedipine, tolerated heavier work loads after receiving the drug, with a more marked increase in flow during exercise. It is concluded that variable threshold exertional angina can be objectively demonstrated by repeat exercise tests in patients with vasospastic angina. Variability of the angina threshold may be due to a functional mechanism that causes myocardial ischemia in addition to the increased myocardial metabolic requirements provoked by exercise. Because in such patients fluctuations in coronary arterial tone play an important role in determining the response to exercise, calcium antagonistic drugs, which lower coronary tone and prevent the occurrence of coronary spasm, are effective in increasing exercise capacity.

Adult↗

Effects of nifedipine on coronary hemodynamic findings during exercise in patients with stable exertional angina.

To investigate the mechanism by which nifedipine improves exercise tolerance in patients with coronary artery disease, we studied 14 patients with stable exertional angina and left anterior descending artery disease by measuring great cardiac vein flow (GCVF) and calculating anterior regional coronary resistance (ARCR) during exercise before and after sublingual administration of 20 mg of nifedipine. After nifedipine seven patients (group I) had no increase in exercise capacity and showed a similar magnitude of ST segment depression at peak exercise, while another seven patients (group II) had prolonged exercise duration (p less than .001) with less ST segment depression at peak exercise (p less than .01). Such effects were achieved despite a significant increase in double product, an indirect index of myocardial oxygen consumption. In group I patients no significant change was induced by nifedipine in GCVF or in ARCR either at rest or at peak exercise. In contrast, in group II patients nifedipine significantly increased GCVF at rest (p less than .05) and at peak exercise (p less than .001). Moreover, resting ARCR was decreased (p less than .01) and remained significantly lower at peak exercise (p less than .01) compared with the prenifedipine values. These data show that nifedipine may increase GCVF and decrease ARCR at rest and at peak exercise in patients with left anterior descending artery disease. Such increase in myocardial oxygen supply seems the most likely mechanism by which nifedipine may improve exercise capacity in patients with stable exertional angina.

Adult↗

Variable threshold of angina during exercise: a clinical manifestation of some patients with vasospastic angina.

Two patients complained of chest pain while at rest and during physical activities. However there seemed to be no direct relation between exertional angina and an increasing level of work performed, indicating that these patients had a variable threshold of angina during exercise. In one patient spontaneous chest pain was associated with transient S-T segment changes in precordial leads, and during coronary arteriography the administration of ergonovine induced spasm of the left anterior descending coronary artery. The other patient showed S-T segment elevation in inferior leads during an ergonovine-induced anginal attack and coronary arteriography revealed a spontaneous spasm of the right coronary artery. In both patients repeated exercise tests yielded different results, because the chest pain and S-T segment depression occurred at different work loads with large differences in heart rate-systolic blood pressure product. It is concluded that a variable threshold of angina during exercise is a clinical manifestation in some patients with vasospastic angina and is probably due to the difference in coronary arterial tone at the onset of exercise.

Angina Pectoris↗

Significance of exercise-induced ST-segment elevation in patients without myocardial infarction.

Sixteen patients with exercise-induced ST-segment elevation and without a history of myocardial infarction or left ventricular aneurysm were studied. Fourteen complained of angina at rest, which was associated with ST-segment elevation in the same leads where it was recorded during exercise, and two patients had only exertional angina. Exercise-induced ST-segment elevation was generally reproducible in subsequent exercise tests performed in different hours of the day, but exercise tests repeated a mean of 15 months later did not induce this electrocardiographic abnormality. All patients had a marked susceptibility to coronary spasm, as shown by the response to the ergonovine test (12 positive tests in 12 patients) and by the occurrence of spontaneous spasm during coronary arteriography in two patients. In addition, coronary arteriography, performed in seven patients at the time of exercise-induced ST-segment elevation, revealed spasm of a major coronary vessel in all. In two patients we documented that exercise-induced ST-segment elevation was accompanied by a decreased coronary blood flow and increased coronary vascular resistance. We conclude that exercise-induced ST-segment elevation in patients without a history of myocardial infarction or left ventricular aneurysm is caused by coronary spasm of a major coronary vessel.

Adult↗

Coronary arterial spasm in angina at rest associated with transient ST-segment changes.

In order to clarify the role of coronary arterial spasm in the pathogenesis of angina at rest, coronary arteriography was perforned during spontaneous chest pain or following intravenous administration of ergonovine maleate in 40 patients with angina at rest. Coronary vasospasm was demonstrated in 23 patients with ST-segment elevation during chest pain (group I), in 7 with ST-segment depression (group II), and in 4 with both ST-segment depression and elevation (group III). Complete spastic occlusion of the proximal or of the midportion of the left anterior descending artery was always associated with ST-segment elevation in anterior leads. In contrast, transient ST-segment depression in anterior leads was associated with diffuse narrowing of the left anterior descending artery with slow progression of the contrast medium, or complete occlusion of a small branch or of the distal segment of the left anterior descending artery. ST-segment elevation in inferior leads was associated with complete spastic occlusion or with significant spastic narrowing of the right coronary artery or of the circumflex artery. We conclude that coronary spasm can be demonstrated in a selected cohort of patients with angina at rest associated with transient ST-segment changes. In some cases the site and the severity of the spasm may produce varying degrees of ischemia, thus determining the direction of the ST-segment shift.

Adult↗

Favorable effects of hyaluronidase on electrocardiographic evidence of necrosis in patients with acute myocardial infarction.

To evaluate hyaluronidase's effect in reducing post-infarction myocardial necrosis, we randomized 91 patients with anterior infarction to control (45) or to hyaluronidase-treatment (46) groups. A 35-lead precordial electrocardiogram was recorded on admission and seven days later. Hyaluronidase was administered intravenously after the first electrocardiogram and every six hours for 48 hours. QRS-complex changes were analyzed to assess the drug's effect. Precordial sites with ST-segment elevation (larger than or equal to 0.15 mV) on the initial electrocardiogram that retained an R wave were considered vulnerable for the development of electrocardiographic signs of necrosis. The sum of R-wave voltages of vulnerable sites fell more in the control group than in the hyaluronidase group (70.9 +/- 3.6 per cent [+/- 1 S.E.M.] vs 54.2 +/- 5.0 per cent P less than 0.01). Q waves appeared in 59.3 +/- 4.9 per cent of the vulnerable sites in control versus 46.4 +/- 4.9 per cent in hyaluronidase-treated patients (P less than 0.05). Thus, hyaluronidase reduced the frequency of electrocardiographic signs of myocardial necrosis.

Acute Disease↗

Comparison of quinidine plasma concentration curves following oral administration of some short- and long-acting formulations.

1 The time-course of quinidine plasma concentrations and selected kinetic parameters were studied in healthy male volunteers given single oral doses of four different quinidine formulations. Comparison was made with quinidine sulphate in a rapidly dissolving form. 2 Plasma half-lives did not significantly differ among treatments. 3 Quinidine polygalacturonate appears to be equivalent to quinidine sulphate in respect to both the absorption and elimination kinetics. When both quinidine bisulphate (Kinidin Durules) and quinidine arabogalactansulphate (Longacor) were administered plasma levels peaked significantly later than after quinidine sulphate. However, while the former seems to be absorbed to the same extent as quinidine sulphate, the latter exhibits lower bioavailability in respect to all other preparations.

Administration, Oral↗