Search PubMed⌕ Search

Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 343 records · Page 19Linked to original sources

Effects of verapamil in preventing early postinfarction angina and reinfarction.

Because verapamil is effective in the treatment of "preinfarction" angina, a single-blind, placebo-controlled trial was performed in 17 patients admitted to the coronary care unit with transmural acute myocardial infarction (AMI) to assess the effects of verapamil on angina and reinfarction after AMI. The study was terminated because results obtained in the initial 17 patients indicated that verapamil is not as effective in treating angina after AMI as it is in angina before AMI and does not prevent reinfarction. Continuous electrocardiographic monitoring during the first 3 days after AMI showed the presence of transient episodes of ST-segment elevation in 4 patients taking verapamil and 4 patients taking placebo. The total number and duration of transient ischemic episodes was similar in the 2 groups (46 vs 41 and 23 +/- 22 vs 17 +/- 15 minutes, respectively). The percentage of transient ischemic episodes accompanied by chest pain was similar in both groups (10%). The ischemic episodes were never preceded by important increases of heart rate. Four patients taking verapamil and 4 taking placebo had reinfarction within the first 10 days after the incident AMI. These findings suggest that the prevailing mechanisms of myocardial ischemia in the immediate post-AMI period could be different from those operating in angina before AMI.

Aged↗

Improved coronary supply: prevailing mechanism of action of nitrates in chronic stable angina.

Exercise tolerance before and after sublingual isosorbide dinitrate (ISDN), 10 mg, was assessed in 217 consecutive patients with stable angina, positive exercise test, and angiographically proved coronary artery disease. In 65 patients (30%), ISDN prevented exercise-induced ST segment depression and/or increased exercise time to 1 mm ST segment depression (greater than or equal to 3 minutes), despite the significantly higher (greater than or equal to 25 X 10(2) increment) rate-pressure product attained (increased coronary reserve). On the contrary, in 40 other patients, exercise test remained positive, and neither time to 1 mm ST segment depression nor rate-pressure product increased significantly (fixed coronary reserve). The remaining 106 patients had an intermediate response. To assess the mechanisms underlying the beneficial action of nitrates, we further investigated 13 patients with increased coronary reserve (group 1) and five with fixed coronary reserve (group 2) by the exercise response to ISDN and verapamil, the changes in left ventricular volumes after ISDN and verapamil, the ECG response to intravenous ergonovine, and the changes in coronary stenosis severity following intravenous ergonovine and intracoronary nitrates. ISDN dramatically improved exercise capacity only in group 1 patients. However, it induced a significant reduction of left ventricular volumes in both groups (p less than 0.01). Ergonovine provoked angina and ST segment depression in 62% of group 1 patients and significantly increased the severity of their coronary stenoses (p less than 0.01). In all group 2 patients, ergonovine was negative, and no significant increase in stenosis severity was observed. Intracoronary nitrates reduced stenosis severity in group 1 (p less than 0.01) but not in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Failure of experimental atherosclerosis to sensitize coronary arteries to spasm in hypercholesterolemic rabbits.

Since hypercholesterolemia sensitizes isolated rabbit coronary arteries to vasoconstrictor stimuli, we assessed the possibility of reproducing occlusive coronary spasm both in vitro and in vivo in atherosclerotic rabbits. In Langendorff-perfused hearts from nine atherosclerotic rabbits (2% cholesterol diet for 18 weeks), despite a threefold increase of cholesterol concentration in the coronary wall compared with nine control rabbits, ergonovine and serotonin did not produce any increase of coronary vascular resistances; the increase produced by pitressin was significantly less in atherosclerotic than in normal hearts (56 +/- 13% vs 138 +/- 28%, p less than 0.05, respectively), whereas that produced by phenylephrine was similar (10.1 +/- 1.8% vs 8.5 +/- 2.4%, p = n.s.). In eight other unanesthetized rabbits we recorded the ECG during ergonovine administration (0.05 mg/kg) and during hypothalamic stimulation before and at regular intervals during the 2% cholesterol diet; rabbits survived for periods ranging from 1 to 22 weeks (mean 9.6 weeks). Only one animal had ST depression during episodes of marked tachycardia; no ischemic ECG changes were ever observed in the other rabbits despite the diffuse subintimal coronary deposition of cholesterol found postmortem. Thus, in atherosclerotic rabbits with chronic marked hypercholesterolemia, coronary arteries do not develop occlusive coronary spasm as observed in patients with variant angina.

Animals↗

Influence of the chosen model of stenosis on pressure-flow relationships in isolated perfused arteries.

Passive changes in luminal diameter caused by a fall in the intravascular distending pressure at the site of a severe coronary artery stenosis were recently proposed as a possible cause of transient myocardial ischaemia. We tested this hypothesis in 5 dog carotid arteries perfused with blood at a constant inflow (100 mm Hg) and variable outflow pressures (40-0 mm Hg). Similar degrees of stenosis were induced either with an external circumferential snare or with an intravascular fluid-filled balloon catheter. In 39 experiments outflow pressure was progressively decreased from 40 to 0 mm Hg. This was done first in the absence of stenosis, secondly with an external stenosis (snare) and finally with an internal stenosis of comparable severity (fluid-filled balloon). When stenosis was absent or intraluminal, flow increased progressively from 109.1 +/- 39 to 136 +/- 55 ml/min (P less than 0.06) and from 23 +/- 16 to 34.2 +/- 16 ml/min (P less than 0.001), respectively. Resistance also rose because flow increased proportionally less than the pressure gradient. Conversely, when stenosis was produced by a snare, flow decreased progressively, from 23.9 +/- 17 to 10.7 +/- 15 ml/min (P less than 0.001). Assuming the reduction of flow was caused by the external stenosis compressing the wall into the lumen (against the intravascular pressure) we prepared an artificial vessel with a foam rubber wall inside a silastic tubing. In this artificial vessel (but not in a glass model) a snare stenosis caused reduction in flow when outflow pressure was lowered. Passive changes in caliber due to a reduced distending pressure do not therefore appear to be a cause of flow reduction.

Animals↗

Role of heart rate in pathophysiology of chronic stable angina.

11 patients with chronic, stable, effort angina, off medication apart from glyceryl trinitrate, were monitored continuously by electrocardiogram (ECG) during normal, unrestricted daily activity. Computerised ECG analysis demonstrated during 33 twenty-four hour periods of monitoring, 278 episodes of transient ischaemic ST segment depression of which 52 were associated with angina. In the 15 minutes preceding the onset of ischaemia, heart rate did not increase in 164 episodes, increased slightly (greater than or equal to 5 beats/min) in 61, and increased moderately or markedly (greater than or equal to 10 beats/min) in 53. Findings were similar when episodes with or without angina or episodes of different severity were analysed separately. In all patients, periods of sinus tachycardia exceeding the control rate by more than 30 beats/min and lasting more than 10 minutes, often occurred in the absence of angina and/or ST segment depression. Also, in 65% of the ischaemic episodes, heart rate at the beginning of the ST change was either below or less than 10 beats/min above the modal value of the twenty-four hour heart rate. This suggests that increased myocardial demand is not necessarily the only or the most common cause of acute ischaemia in patients with chronic effort angina during unrestricted daily activity. Factors which only transiently interfere with myocardial oxygen supply are probably important in this syndrome.

Aged↗

Quantitative radionuclide angiocardiography using gold-195m.

A limitation of first-pass radionuclide angiocardiography is the limited repeatability because of the relatively long half-life of technetium-99m (Tc-99m). The feasibility, reproducibility and validity of multiple sequential quantitative first-pass studies were assessed in humans using the short-lived isotope gold-195m (Au-195m) (half-life of 30.6 seconds, 262 keV), which can be directly obtained from a generator made of its parent isotope, mercury-195m (half-life of 41.6 hours). Thirty-three subjects (13 normal volunteers and 20 cardiac patients) were studied using a large-field gamma camera equipped with a medium-energy collimator. After Au-195m intravenous injections, repeat first-pass studies were performed in the left anterior oblique projection. A left anterior oblique study was then obtained after i.v. injection of Tc-99m. Left ventricular ejection fraction calculations were performed separately by 2 observers. Reproducibility of Au-195m first-pass studies was excellent. The correlation coefficients for left ventricular ejection fraction from the first and the second Au-195m injections were 0.93 and 0.98 for observers 1 and 2, respectively. The correlation coefficients between Au-195m and Tc-99m first-pass studies were 0.95 and 0.98, respectively.

Adult↗

Evaluation of the effects of catheter sampling for the study of platelet behavior in the pulmonary and coronary circulation.

To study the effects of sampling through cardiac catheters on indices of platelet function, we measured the levels of platelet factor 4 (PF4), beta thromboglobulin (BTG), and platelet aggregate ratio (PAR) in 10 patients with atrioventricular accessory pathway (AVNAP), six patients with primary pulmonary hypertension (PPH), and six patients with critical narrowing of the left anterior descending artery (LAD). In AVNAP and LAD patients samples were drawn simultaneously from a peripheral vein, coronary sinus, and brachial artery; in AVNAP patients samples were also obtained from the axillary vein before the coronary sinus was entered. In PPH patients samples were drawn from pulmonary artery, aorta, and a peripheral vein; in these patients the effects of an intravenous infusion of prostacyclin (PGI2) (2 to 8 ng/kg/min) on PF4, BTG, and PAR were also studied at all sampling sites. In all patients arterial, coronary sinus, pulmonary arterial, and axillary venous levels of PF4, BTG, and PAR significantly exceeded those measured in the peripheral vein. PGI2 infusion resulted in a significant decrease of PF4 at all sampling sites, while no consistent BTG changes were observed and PAR levels did not decrease in the peripheral vein. Although a considerable interpatient variability in PF4 levels was observed, a significant (r = 0.91) correlation was found in patients with AVNAP between simultaneous coronary sinus and arterial PF4 levels. The value of PF4 coronary sinus-arterial difference in LAD patients was consistently higher than that calculated in AVNAP patients (54.5 +/- 28.9 vs 4.2 +/- 3.8 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Failure of transdermal nitroglycerin to improve chronic stable angina: a randomized, placebo-controlled, double-blind, double crossover trial.

We assessed the effect of transdermal nitroglycerin (NTG-TTS), releasing 5 mg/24 hr, in 11 patients with chronic stable angina during a randomized, placebo-controlled, double-blind, double crossover trial of four 1-week periods. All patients had a positive exercise test and coronary artery disease prior to entry into the study. Efficacy was assessed weekly by anginal diaries, ambulatory ST segment recordings, and computerized exercise testing 2 to 4 hours after renewal of NTG-TTS. One patient withdrew in the first week (placebo) and was excluded from all analysis. The weekly frequency of anginal attacks was 9 +/- 11 (mean +/- SD) and 9 +/- 10 during the 2 placebo weeks and 11 +/- 14 and 9 +/- 11 during NTG-TTS; the time to 1 mm ST segment depression (seconds) was 268 +/- 178 and 303 +/- 217 with placebo and 228 +/- 221 and 285 +/- 178 with NTG-TTS; exercise duration (seconds) was 375 +/- 230 and 467 +/- 254 during placebo and was 394 +/- 233 and 412 +/- 236 during NTG-TTS. The weekly number of episodes of ST depression was 11 +/- 9 and 8 +/- 5 during placebo and 8 +/- 5 and 9 +/- 7 during NTG-TTS. Our study failed to show any consistent differences in patients treated with placebo or NTG-TTS.

Administration, Topical↗

Computer system for analysis of ST segment changes on 24 hour Holter monitor tapes: comparison with other available systems.

The accuracy of a computer system that was developed for the analysis of ST segment changes recorded on Holter ambulatory electrocardiographic monitoring tapes was compared with conventional visual scrutiny, beat by beat analog printouts and a commercial J point trend system. The program calculates and plots multiple electrocardiographically derived variables in a high temporal resolution trend format. Fifty tapes of good recording quality obtained from 19 patients (13 with chronic stable angina and 6 with variant angina) were assessed visually and with the computer system; of these, 20 were analyzed by all four techniques. In the 50 tapes, 629 episodes of diagnostic ST segment changes (all true positive results) were identified by using the computer system. In contrast, only 507 were identified by visual scrutiny; none of these 507 episodes was missed by computer analysis. On the 20 tapes assessed using computer, visual, beat by beat analog and J point trend system analysis, 268, 221, 230 and 178 episodes, respectively, were documented. For the four techniques, false negative and positive results were 0, 47, 38 and 90 and 0, 10, 6 and 24, respectively. The results indicate that, of the systems assessed in this study, the computer program provides the highest accuracy for detection of transient ST segment changes. This is probably accreditable to the compact presentation of multiple electrocardiographically derived variables, allowing a detailed quantitative assessment of 24 hour tapes. It is of particular value for pathophysiologic and pharmacologic studies.

Angina Pectoris↗

Unreliability of conventional visual electrocardiographic monitoring for detection of transient ST segment changes in a coronary care unit.

Visual monitoring at the central station of coronary care units (CCUs) may not adequately assess the presence and frequency of transient asymptomatic ST segment changes in patients with unstable angina. We have performed continuous 24-h electrocardiographic recordings over a total period of 50 days in 10 patients admitted to our CCU with frequent attacks of angina at rest. Over the corresponding period, at the central monitoring station (6 beds), the nursing-staff detected only 31 transient ischaemic episodes (27 with ST elevation, 4 with depression, 9 of which were asymptomatic). By contrast the retrospective analogue analysis of tapes identified 213 ischaemic episodes: 143 with ST elevation (greater than or equal to 0.2 mV) and 70 with ST depression (greater than or equal to 0.2 mV); usual CCU monitoring failed to report changes during 13 episodes (8 with ST elevation, 5 with depression) accompanied by anginal pain. When the tapes were played back in real time on a CCU monitoring scope, a cardiologist (who had the option of interrupting the play-back whenever tired) recognized 48% of the episodes when presented in groups of 4 and randomly positioned on the screen together with 2 other electrocardiographic tracings not related to the study; he recognized 92% of the episodes when only one ECG was presented on the screen. Thus conventional visual monitoring in a CCU considerably underestimates the incidence of transient ischaemic ST segment changes, some of which were accompanied by pain. This low rate of detection is the result of the presentation on the central monitoring station of several ECGs and of fatigue.

Adult↗

Regional pulmonary blood volume in patients with abnormal blood pressure or flow in the pulmonary circulation.

We studied the effects of a chronic increase in flow and of chronic hypertension on regional pulmonary blood volume and extravascular lung density (lung tissue and interstitial water per unit thoracic volume) in one group of patients with intracardiac, left-to-right shunt and in another group with Eisenmenger's syndrome or primary pulmonary hypertension. We used positron computerized tomography to measure regional lung density (transmission scans) and blood volume (labelling with 11CO). The distribution of pulmonary blood volume was more uniform in patients with a chronic increase in pulmonary blood flow than in normal subjects. There were also indications of an absolute increase in intrapulmonary blood volume. In patients with chronic pulmonary arterial hypertension, the regional distribution of blood volume was abnormally uniform, but there were no indications of substantial abnormalities in overall intrapulmonary blood volume.

Adolescent↗

Spasm and dynamic coronary stenoses.

Spasm is only one type of dynamic stenosis typically responsible for variant angina; spasm with or without transient intraluminal plugging, superimposed on a wide range of old or fresh, fixed stenoses, is largely responsible for unstable angina; physiological changes of tone around pliable coronary stenoses probably account for the variable exercise tolerance and for spontaneous attacks in patients with stable angina. Sustained spasms, not responsive to nitrates and thrombosis, are likely to be involved at different times or simultaneously in acute coronary occlusion causing myocardial infarction. Acute or worsening phases of coronary diseases are largely caused by dynamic stenoses, whereas stable, fixed-threshold, predictable angina may be the only feature of quiescent phases of coronary disease.

Angina Pectoris↗

alpha-Adrenergic receptors and coronary spasm: an elusive link.

In 14 consecutive patients with variant angina we investigated the possible role of coronary alpha-adrenergic receptors in the genesis of coronary spasm. In eight patients, computerized, beat-by-beat analysis of the electrocardiogram recorded during continuous Holter monitoring failed to reveal any increase of heart rate and corrected QT interval (both indexes of cardiac sympathetic activation) in the period preceding the onset of ST segment changes in 197 episodes of ischemia caused by coronary spasm. In the same patients, analysis of the circadian distribution of ischemic episodes revealed a significantly higher incidence in the early morning hours, when sympathetic activity is at the lowest level. Twelve patients underwent serial provocative testing with cold pressor, phenylephrine, or norepinephrine infusion and administration of ergonovine maleate. Ergonovine consistently reproduced coronary spasm in all 12 patients, while results of cold pressor testing were positive in only one. Infusion of phenylephrine (eight patients) or norepinephrine after beta-blockade (four patients) failed to precipitate myocardial ischemia. In five patients infusion of phentolamine at the highest tolerated dose did not reduce significantly the number of ischemic attacks when compared with placebo. In contrast to results of previous reports, our data seem to rule out the hypothesis that an increase of sympathetic outflow to the heart plays an important role in the genesis of coronary spasm. We cannot, however, exclude the possibility of localized alpha-stimulation of epicardial arteries.

Adult↗