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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 307 records · Page 17Linked to original sources
PubMed1987

Usefulness of Holter monitoring to improve the sensitivity of exercise testing in determining the degree of myocardial revascularization after coronary artery bypass grafting for stable angina pectoris.

To assess whether Holter monitoring improves the sensitivity of exercise testing in identifying incomplete myocardial revascularization, both tests were performed in 45 patients from 3 to 5 months after elective coronary artery bypass grafting (CABG) for stable angina pectoris. Coronary angiography revealed incomplete revascularization in 26 patients. Six of these 26 had 52 episodes of ST-segment depression during Holter monitoring and myocardial ischemia during exercise testing. Their exercise capacity was significantly lower than that of 10 other patients in whom the results of exercise testing only were positive (heart rate at 0.1 mV ST-segment depression 112 +/- 9 vs 123 +/- 15 beats/min, p less than 0.001). In the other 10 patients with incomplete myocardial revascularization the results of both investigations were negative. The graft patency rate was lower in patients with a positive response to exercise testing than in those with a negative response (52% vs 71%, p less than 0.005). Myocardial revascularization was angiographically complete in 19 patients. In 18 of these 19 patients the findings of both investigations were negative; in 1 patient Holter monitoring revealed episodes of ST-segment elevation suggestive of variant angina. Thus, after CABG for stable angina pectoris the results of Holter monitoring do not improve the sensitivity of exercise testing in identifying patients with angiographically incomplete myocardial revascularization because findings are positive only in patients with low exercise capacity. Both tests fail to show evidence of myocardial ischemia in most patients with angiographically complete myocardial revascularization.

Aged↗
PubMed1987

Increase in S-wave amplitude during ischemic ST-segment depression in stable angina pectoris.

In 50 patients with chronic stable angina and in 10 asymptomatic young male volunteers, the behavior of S-wave amplitude was studied during episodes of ischemic ST-segment depression, both induced by exercise testing and occurring during ambulatory electrocardiographic monitoring. With exercise, all patients showed diagnostic ST-segment depression (0.16 +/- 0.05 mV) which, in 49, was associated with an increase in S-wave amplitude. No consistent changes in R-wave amplitude were observed. S-wave amplitude also increased in all control subjects during exercise, but the sum of R and S wave remained constant, while it increased in 42 patients. In the 10 study patients undergoing Holter monitoring we identified 170 episodes of ischemic ST-segment depression, of which 169 were associated with increased S-wave amplitude. Isolated increases in S-wave amplitude without ST-segment changes occurred in 3 of 4 normal subjects. Dipyridamole echocardiography revealed regional wall motion abnormalities in 12 of 21 patients; the changes were invariably associated with increased S-wave amplitude but not necessarily with diagnostic ST-segment depression. An increase in S-wave amplitude is almost invariably associated with subendocardial ischemia, sometimes in the absence of ST-segment changes; this sign could represent a sensitive (although less specific) additional marker of myocardial ischemia.

Adult↗
PubMed1987

Coronary artery infusion of neuropeptide Y in patients with angina pectoris.

Neuropeptide Y was infused into a coronary artery of 6 patients with typical angina but no significant coronary stenosis. 3 patients had transient myocardial ischaemia, shown by typical pain and electrocardiographic change, at doses of 0.2 pmol/kg per min in 2 patients and 1.0 pmol/kg per min in 1 patient. The arteriographic appearances suggested constriction of small vessels rather than constriction of epicardial coronary arteries. The ischaemia was completely reversed by intracoronary administration of isosorbide dinitrate with no adverse sequelae. This is the first demonstration of myocardial ischaemia in man induced by a peptide neurotransmitter.

Adult↗
PubMed1987

Limitations of dipyridamole-echocardiography in effort angina pectoris.

The sensitivity of dipyridamole--2-dimensional (2-D) echocardiography was assessed for detection and localization of ischemia in 21 patients with severe chronic stable angina pectoris, a clearly positive exercise stress test response and multivessel coronary atherosclerosis. Regional wall motion during dipyridamole infusion (0.6 mg/kg intravenously over 4 minutes) was compared with control and recovery by 2 blinded observers in consensus. Transient regional wall motion abnormalities were observed in 11 patients. Angina and ST-segment changes occurred in 9 of these 11 patients with positive responses, but in none of those who showed no transient abnormality of regional wall motion. Localization of regional wall motion abnormalities correlated well with angiographic severity of coronary lesions. Endocardial area contraction, evaluated by a computerized system, was reduced significantly after dipyridamole administration in patients with a positive response (from 51 +/- 10% to 35 +/- 11%, p less than 0.001), whereas it did not change significantly in the others (from 43 +/- 6% to 42 +/- 8%). In the 11 patients with a positive response, coronary reserve assessed by exercise testing (modified Bruce protocol) was more impaired than in those with a negative response (time to 1 mm of ST depression 177 +/- 148 seconds and 472 +/- 179 seconds, respectively, p less than 0.01). In patients with severe angina and multivessel coronary artery disease, dipyridamole--2-D echocardiography appears to identify the vessel in which flow reserve is most limited. Although this information may be valuable, indications for the test are restricted to patients with severely limited exercise capacity.

Adult↗
PubMed1987

Louis F. Bishop lecture. Role of coronary artery spasm in symptomatic and silent myocardial ischemia.

The revival of the concept of coronary spasm has stimulated research into coronary artery disease. Observations in patients with variant angina have substantially contributed to the appreciation of painless myocardial ischemia. However, the presence or absence of pain during ischemic episodes is not related to the cause of ischemia, because painless ischemia can be observed in variant angina (caused by spasm), in effort-induced angina (caused by increased myocardial demand) and in myocardial infarction (caused by thrombosis). Continuous monitoring initially of patients with variant angina and subsequently of patients with unstable and stable angina proved that often painful and painless ischemic episodes are caused by a transient impairment of regional coronary blood flow rather than by an excessive increase of myocardial demand. The transient impairment of coronary flow appears to be caused by dynamic stenosis of epicardial coronary arteries. This most often occurs at the site of atherosclerotic plaques encroaching on the lumen to a variable extent. Dynamic stenosis can be caused by 1) "physiologic" increase of coronary tone, as in stable angina, 2) spasm, as in variant angina, and 3) thrombosis, usually in combination with "physiologic" changes in tone or with spasm, or both, as in unstable angina. The mechanisms of spasm, as typically observed in variant angina, are different from those of "physiologic" increase of tone; they appear to be related to a local alteration that makes a segment of coronary artery hyperreactive to a variety of constrictor stimuli causing only minor degrees of constriction in other coronary arteries. The nature of this abnormality, which may remain stable for months and years, is yet unknown.

Angina Pectoris, Variant↗
PubMed1987

Effect of nifedipine on myocardial metabolism in patients with unstable angina.

Myocardial glucose metabolism was assessed using 18F-fluorodeoxyglucose and positron emission tomography in 6 normal volunteers, 7 patients with coronary artery disease and stable angina and 15 patients with unstable angina. All studies were carried out on resting, fasting patients. The patients were off treatment and had no evidence of acute myocardial necrosis or ischaemia. A second study investigated the myocardial glucose metabolism of 5 of the patients with unstable angina after treatment with oral nifedipine. In the first study, the metabolic rate for glucose (MRG) was found to be similar in patients with stable angina and normal volunteers (0.023 +/- 0.032 vs 0.012 +/- 0.008 mumol ml-1 min-1, P less than 0.42), whereas the MRG was significantly higher in patients with unstable angina compared with both that of normal volunteers and patients with stable angina (0.084 +/- 0.047 mumol ml-1 min-1, P less than 0.001). In the second study, the MRG of all of the 5 patients with unstable angina studied after the administration of nifedipine was significantly reduced (P less than 0.05), but was still higher than that of the normal controls. The possibility of spontaneous metabolic changes cannot be excluded, but the consistent reduction of the MRG in all 5 patients after the administration of nifedipine suggests that nifedipine has a beneficial effect on myocardial metabolism that could be related to either an increase in myocardial blood flow or to a direct metabolic effect of nifedipine.

Adult↗
PubMed1987

Regional extravascular density of the lung in patients with acute pulmonary edema.

The regional distribution of extravascular lung density (lung tissue and interstitial or alveolar fluid per unit thoracic volume) and fractional pulmonary blood volume (volume of blood per unit thoracic volume) was measured in five patients with acute interstitial pulmonary edema and two patients with acute alveolar edema. We found a uniform increase in extravascular lung density in the patients with acute interstitial edema but a preferentially dependent distribution in the patients with alveolar edema. Fractional blood volume had an abnormally uniform distribution in patients with interstitial edema. In alveolar edema, there was marked redistribution of blood volume away from severely edematous regions. The results are in agreement with previous experimental work with animal models. The distribution of extravascular lung density and fractional blood volume in subjects with acute interstitial edema is, however, different from that found in subjects with chronic interstitial edema, suggesting that the pathophysiological characteristics of the two conditions may be different.

Acute Disease↗
PubMed1987

Induction of coronary artery spasm by a direct local action of ergonovine.

To investigate whether ergonovine acts directly on coronary arteries or via remote neurohumoral reflexes, we administered small titrated increments of intracoronary ergonovine up to a maximum cumulative dose of 50 micrograms to 15 patients. In six patients with variant angina (group 1), ischemic electrocardiographic ST changes, angina, and localized coronary spasm (local coronary diameter reduction of 87.8 +/- 18.9% [mean +/- SD]) followed after 6 to 50 micrograms (mean 20.7) cumulative intracoronary ergonovine. In nine patients with atypical chest pain, normal baseline coronary arteriograms, and no evidence of variant angina (group 2), there was no ischemic ST segment change or localized coronary spasm after 6 to 50 micrograms (mean 31.6) intracoronary ergonovine. Coronary diameter of proximal vessels of patients in group 2 was reduced by 16.2 +/- 6.5% and did not differ from the response of nonspastic vessels of comparable size of group 1 (20.5 +/- 13.8%; p = .7). There was no significant difference in the median effective dose values in the dose-response curves of the spastic and nonspastic segments between groups 1 and 2. Ergonovine causes coronary spasm by a direct local effect, which seems to be caused by localized arterial hyperreactivity rather than supersensitivity. Intracoronary delivery may be safer than intravenous administration because negligible drug recirculation may prevent perpetuation of spasm and selective coronary administration can avoid branches with critical stenoses.

Coronary Vasospasm↗
PubMed1987

Efficacy of carvedilol in exercise-induced myocardial ischemia.

The exercise response to a single oral dose (25 mg) of a new beta-blocking agent that also has potent vasodilating properties, carvedilol, was assessed in 15 patients with stable exertional angina, positive exercise tests (greater than or equal to 1 mm ST depression) and coronary artery disease. A placebo-controlled, randomized, crossover study was carried out. Compared with placebo, carvedilol significantly reduced both resting heart rate (HR) and blood pressure (BP) at rest. After the administration of carvedilol, 10 of the 15 patients did not have angina at peak exercise and 5 had ST shifts less than 1 mm. Total exercise time and time to 1 mm ST depression were prolonged, and ST segment depression at peak exercise was significantly reduced. Systolic BP was reduced both at peak exercise and at 1 mm ST depression whereas mean HR at peak exercise did not change significantly compared with placebo. Overall, mean HR-BP product at peak exercise was significantly reduced by carvedilol compared with placebo. However, four patients achieved similar or higher HR-BP product and yet did not experience angina and had less ST depression (or no ST segment shifts) during exercise. This indicates an increase in their coronary flow reserve. These results suggest that carvedilol is effective therapy for effort-induced angina, and this may be related to its combined beta-blocking and vasodilatory properties.

Adrenergic beta-Antagonists↗
PubMed1986

Transient myocardial ischemia during daily life in patients with syndrome X.

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 +/- 18 vs 117 +/- 18 beats/min, p less than 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, myocardial ischemia frequently develops during daily life; silent ischemia is an important component of this syndrome; and increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.

Adult↗
PubMed1986

Importance of generalized defective perception of painful stimuli as a cause of silent myocardial ischemia in chronic stable angina pectoris.

Growing evidence indicates that most patients with coronary artery disease frequently have episodes of painless myocardial ischemia. Previous studies from our institution show that the severity and duration of myocardial ischemia are necessary but not sufficient factors to explain the occurrence of anginal pain. The responses to a battery of painful stimuli were studied in 12 patients with predominantly painless (group A) and in 15 patients with predominantly painful (group B) ischemic episodes. The severity of myocardial ischemia as assessed by the measurement of ST-segment depression during exercise stress testing and during ambulatory electrocardiographic monitoring was comparable in the 2 groups. Patients in group A had a significantly higher threshold and tolerance for forearm ischemia (+32%, p less than 0.05; +120%, p less than 0.001), cold (+100%, p less than 0.05; +180%, p less than 0.01) and electrical skin stimulation (+145%, p less than 0.01; +109%, p less than 0.01), but the overlap between the 2 groups was often appreciable. In the 6 patients with the longest tolerance times for forearm ischemic pain (all in group A) and in the 5 having the shortest tolerance times (all in group B), plasma levels of beta endorphin, met-enkephalin, noradrenaline and adrenaline were similar during both the basal state and the induction of forearm ischemic pain. Thus, a generalized defective perception of painful stimuli plays an important role in many patients with predominantly painless myocardial ischemia. Other mechanisms, however, may also be important, particularly in patients whose threshold and tolerance values overlap with those of patients who have predominantly painful myocardial ischemia.

Angina Pectoris↗
PubMed1986

Pathogenetic classifications of unstable angina as a guideline to individual patient management and prognosis.

Although it is widely recognized that unstable angina is a syndrome encompassing a variety of clinical and pathophysiologic entities, clinical trials and guidelines for management still consider patients with unstable angina as a single homogeneous group. When first recognized as a potentially threatening coronary syndrome, unstable angina was thought to be caused by extremely severe coronary obstructions that culminated in the syndrome of angina at rest, when coronary flow reserve is practically exhausted. It is now clear that the severity of coronary atherosclerosis in stable and unstable angina is, on the average, similar; and it appears that the features of "instability" are largely determined by dynamic obstructions superimposed on a widely variable fixed obstruction. Current clinical classifications, although based on purely descriptive symptoms, and angiographic classifications, based solely on coronary anatomy, independently identify subgroups of patients with unstable angina who have clearly distinct prognoses. The pathophysiologic classification proposed in this article considers both the severity of the underlying coronary fixed obstructions (as evidenced by the reduction of coronary flow reserve and by coronary anatomy) and the tendency for dynamic stenoses to develop (as evidenced by the pathophysiologic interpretation of symptoms and by the response to therapy). Since this classification combines elements of currently used clinical and angiographic classifications with a pathophysiologic interpretation, it can be applied easily in clinical practice and may provide more rational groupings of patients for both management and prognosis assessment.

Angina Pectoris↗
PubMed1986

Comparison of verapamil and propranolol therapy for angina pectoris at rest: a randomized, multiple-crossover, controlled trial in the coronary care unit.

The effects of oral verapamil (V), 400 mg/day, oral propranolol (P), 300 mg/day, and placebo were compared in 10 patients admitted to the coronary care unit because of frequent attacks of angina at rest. Testing was done according to a randomized, double-blind, multiple-crossover, placebo-controlled trial, consisting of 8 consecutive 48-hour treatment periods with V or P or placebo. Three patients had variant angina, 5 had episodes of both ST-segment elevation and depression and 2 had only ST-segment depression. One patient had no critical coronary stenoses, 1 had 1-vessel disease, 7 had 2-vessel disease and 1 had 3-vessel disease. Electrocardiographic monitoring and tape recording were continued during the 16 days of the trial. A total of 1,602 episodes of transient diagnostic ST shift were recorded during the trial (1,309 episodes of ST-segment elevation, 293 of ST-segment depression); 43% were painless. Mean blood levels of V and P at the end of the active phases were 161 +/- 89 and 120 +/- 45 ng/ml, respectively. In the group as a whole, the average number of diagnostic ischemic ST-segment shifts per 24 hours was significantly reduced relative to corresponding placebo periods during V (2.6 +/- 2.4 vs 11.9 +/- 8.6; p less than 0.01) but not during P treatment (11.9 +/- 8.6 vs 12.0 +/- 7.3). Similar statistically significant reductions were observed in the number of anginal attacks and nitroglycerin tablets consumed. Considering individual patients, V reduced ischemic episodes during both active phases in all patients, whereas P was effective only in 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Variability of results during repeat exercise stress testing in patients with stable angina pectoris: role of dynamic coronary flow reserve.

In some patients with stable angina, the variability of results during repeated exercise tests is higher than in others with similar symptoms. The aim of the study was to assess whether this difference can be explained by a different susceptibility of the coronary arteries to vasoconstrictor stimuli. Ten patients (group A) with stable angina, who developed myocardial ischemia (angina and ST segment depression greater than 0.1 mV) following ergonovine-induced coronary constriction, and 10 other patients (group B) with stable angina, but a negative ergonovine test result, were subjected to two treadmill exercise tests. The variability of heart rate and heart rate-blood pressure product at 0.1 mV ST segment depression was significantly higher in group A than in group B (12 +/- 4 vs 4 +/- 4 bpm, respectively, p less than 0.001 and 3366 +/- 1900 vs 930 +/- 960 bpm X mm Hg, respectively, p less than 0.005), such as the variability of heart rate-blood pressure product at the onset of angina (3887 +/- 2400 vs 1428 +/- 1800 bpm X mm Hg, respectively, p less than 0.04). The remaining exercise parameters were always more variable in group A than in group B, but these differences did not achieve statistical significance. Thus patients with stable angina who develop myocardial ischemia in response to ergonovine have a larger variability of results during repeat exercise testing. Such findings could be explained by an enhanced susceptibility to the coronary constrictor effects of exercise resulting in dynamic changes in coronary flow reserve.

Aged↗
PubMed1986

Differential transmyocardial platelet behavior in response to pacing and ergonovine-induced myocardial ischemia.

In 17 anginal patients with critical narrowing of the left anterior descending artery, we studied the effects of acute ischemia, either induced by atrial pacing or by ergonovine, on transmyocardial platelet behavior. Six other patients with atypical chest pain and normal coronary arteries served as controls. Simultaneous arterial and great cardiac vein samples were drawn during control and ischemia to measure the levels of platelet factor four (PF4) and beta-thromboglobulin (BTG). During pacing-induced ischemia the great cardiac vein-arterial differences of PF4 and BTG decreased significantly, indicating a reduced platelet aggregability; no significant changes were observed in the control patients. By contrast, when ischemia resulted from ergonovine-induced spasm of the left anterior descending artery (five patients), the great cardiac vein-arterial differences increased, indicating enhanced platelet aggregability. Again no differences were observed in the patients with a negative ergonovine test. The results of our study suggest that the transcardiac platelet behavior may vary during different ischemic conditions. When ischemia is due to increased myocardial demands and flow is normal or increased, myocardial metabolites released from the ischemic area may oppose platelet aggregation. By contrast, spasm and the stagnant flow resulting from it may enhance platelet aggregation.

Adult↗