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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 325 records · Page 18Linked to original sources
PubMed1986

Myocardial glucose utilization in ischaemic heart disease: preliminary results with F18-fluorodeoxyglucose and positron emission tomography.

Regional myocardial utilization of glucose can be assessed non-invasively in man with the sugar analogue F18-2-fluoro-2-deoxyglucose (FDG) and positron emission tomography (PET). The preliminary observations made in patients with different clinical forms of ischaemic heart disease using FDG and PET are reported. In patients with stable angina pectoris at rest, regional myocardial glucose utilization was comparable to that in normal volunteers whilst an increased utilization of glucose was found in the recovery from exercise-induced ischaemia in the regions that showed an abnormal perfusion during the stress test. These metabolic changes persisted in the recovery phase when all the parameters that were altered during the exercise, including myocardial perfusion, had normalized. In patients with unstable angina, characterized by repeated episodes of spontaneous ST depression, myocardial glucose utilization was regionally or globally increased already at rest in the absence of symptoms or signs of ischaemia at the time of study and most often without evident perfusion abnormalities. In patients with a recent infarction, two different patterns of glucose utilization in the infarcted area have been described: a concordant decrease of myocardial perfusion and glucose utilization; a disproportionately increased glucose utilization relative to perfusion interpreted as an index of the presence of ischaemic, but still viable myocardium.

Angina Pectoris↗
PubMed1986

Coronary blood flow and myocardial perfusion in humans: mechanisms of acute transient myocardial ischemia.

Acute myocardial ischemia in patients may result either from an excessive increase in myocardial oxygen consumption when coronary flow reserve is chronically reduced or from a sudden reduction in coronary flow reserve. The mechanisms of transient reduction in coronary flow reserve are multiple and can consist of an increased vasomotor tone or intravascular plugging by blood constituents. It is possible to recognize these two mechanisms of angina in patients on the basis of history and the results of exercise testing. The majority of patients with angina have ischemic episodes caused by both an excessive increase in demand and by transient impairment of blood supply so that they have a mixed form of angina.

Angina Pectoris↗
PubMed1986

Pathophysiology of coronary occlusion in acute infarction.

Coronary angiography has proved beyond doubt that complete coronary occlusion is the rule in the very early hours of infarction. The 60% to 80% rate of coronary recanalization after thrombolytic therapy has proved that thrombosis is a major component of the occlusion at the time when the procedure is performed a few hours after the onset of symptoms. However, the trigger for coronary thrombosis and the causes of failure of thrombolytic therapy are still a matter of speculation. The relatively rare occurrence of acute coronary occlusion in the life of an individual with even severe coronary disease can be explained on the basis of the necessity of either extremely powerful isolated stimuli, which only occurs rarely, or the casual simultaneous presence in one coronary arterial segment of multiple unfavorable events, such as plaque fissuring, enhanced reactivity of coronary smooth muscle to constrictor stimuli and displacement of the thrombotic-thrombolytic equilibrium toward thrombosis. Coronary artery constriction possibly caused by vasoconstrictor substances released by thrombus, represents the potential element of a vicious cycle causing persistent coronary occlusion and reocclusion when reflow occurs with thrombolysis.

Anticoagulants↗
PubMed1986

Increased uptake of 18F-fluorodeoxyglucose in postischemic myocardium of patients with exercise-induced angina.

Regional myocardial perfusion and exogenous glucose uptake were assessed with rubidium-82 (82Rb) and 18F-2-fluoro-2-deoxyglucose (FDG) in 10 normal volunteers and 12 patients with coronary artery disease and stable angina pectoris by means of positron emission tomography. In patients at rest, the myocardial uptake of 82Rb and FDG did not differ significantly from that measured in normal subjects. The exercise test performed within the positron camera in eight patients produced typical chest pain and ischemic electrocardiographic changes in all. In each of the eight patients a region of reduced cation uptake was demonstrated in the 82Rb scan recorded at peak exercise, after which uptake of 82Rb returned to the control value 5 to 14 min after the end of the exercise. In these patients, FDG was injected in the recovery phase when all the variables that were altered during exercise, including regional myocardial 82Rb uptake, had returned to control values. In all but one patient, FDG accumulation in the regions of reduced 82Rb uptake during exercise was significantly higher than that in the nonischemic regions, i.e., the ones with a normal increment of 82Rb uptake on exercise. In the nonischemic areas, FDG uptake was not significantly different from that found in normal subjects after exercise. In conclusion, myocardial glucose transport and phosphorylation seem to be enhanced in the postischemic myocardium of patients with exercise-induced ischemia.

Adult↗
PubMed1986

Provocation of coronary spasm by dopamine in patients with active variant angina pectoris.

The effects of dopamine on arteries are different depending on the dose, route of administration, and receptor population. Its administration can cause vasodilation by stimulation of dopaminergic receptors, vasoconstriction by stimulation of alpha-adrenergic and serotonergic receptors, and even spasm of cerebral arteries when given intracisternally in dogs. The ability of dopamine to provoke coronary spasm was assessed in 18 patients with active vasospastic angina in whom this amine was infused at rates of 5, 10, and 15 micrograms/kg/min for periods of 5 min each. The 12-lead electrocardiogram and blood pressure (cuff) were monitored throughout the whole test. In nine patients dopamine caused angina and ischemic electrocardiographic changes suggestive of coronary spasm: ST segment elevation in six patients and ST segment depression in the absence of important coronary stenoses in the remaining three. Infusion of dopamine was repeated during coronary angiography in three patients with positive test results: this provoked occlusive coronary spasm with ST segment elevation in two patients and nonocclusive spasm with ST segment depression in the remainder. In conclusion, infusion of dopamine provokes coronary spasm in a sizeable proportion of patients with active vasospastic angina. Its administration may be detrimental in patients susceptible to coronary spasm, such as those with acute myocardial infarction.

Adult↗
PubMed1986

Calcitonin gene-related peptide: a potent dilator of human epicardial coronary arteries.

To investigate the action of calcitonin gene-related peptide (CGRP) on human epicardial coronary arteries, six patients received intracoronary CGRP at doses of 50,100, and 200 ng/min. The effect of CGRP was measured angiographically with a computerized analysis system. A dose-dependent increase in coronary arterial diameter was observed. At the highest dose there were 34%, 7%, 38%, and 40% mean increases in the diameters of the circumflex, proximal, mid, and distal left anterior descending arteries, respectively. No further increase in diameter was found after a subsequent dose of 1 mg intracoronary isosorbide dinitrate. Prior infusion of CGRP did not prevent coronary arterial spasm induced by ergonovine in two patients with variant angina, but a subsequent bolus of CGRP partially relieved the spasm. We propose that CGRP has a role in the regulation of coronary vascular smooth muscle tone.

Angina Pectoris↗
PubMed1986

Local coronary supersensitivity to diverse vasoconstrictive stimuli in patients with variant angina.

It has been shown in different groups of patients with variant angina that coronary spasm can be reproduced by physiologic maneuvers and pharmacologic agents. It is not known, however, to what extent different stimuli can induce spasm in the same patient. To investigate whether coronary arterial spasm results from specific abnormal agonist-receptor interactions or from a local nonspecific coronary supersensitivity to different stimuli, 28 patients with vasospastic angina were submitted to a series of diverse vasoconstrictive stimuli known to provoke coronary spasm. Ergonovine, hyperventilation, handgrip, cold pressor, and exercise-tests, were carried out in all 28 patients. In the last 15 patients histamine was also administered. Spasm was provoked by ergonovine in 96% of patients, by hyperventilation in 54%, by histamine in 47%, by exercise in 46%, and by the cold pressor and handgrip tests in 11% and 7%, respectively. No significant differences were found in the responses to provocative tests of patients with normal coronary arteries or nonsignificant stenoses and those with significant lesions. In the same individual, spasm was induced by at least two vasoconstrictive stimuli, although with a different mechanism of action, in 82% of patients and spasm was induced by three or more stimuli in 39%. Tests were repeated in at least 23 patients and short-term reproducibility paralleled sensitivity. These results suggest that in patients with variant angina, a local nonspecific supersensitivity rather than an abnormal specific agonist-receptor interaction plays a major role in the genesis of coronary arterial spasm.

Adult↗
PubMed1986

The fractional distribution of the cardiac output in man using microspheres labelled with technetium 99m.

To investigate the distribution of organ blood flow in patients we have developed a method of quantitating the whole-body fractional distribution of 99Tcm-labelled microspheres. The microspheres were injected into the left ventricle in nine patients with normal cardiac indices (greater than 3 1/min/m2; Group A) and 11 patients with low cardiac indices (less than 2.51 l/min/m2; Group B). The fractional organ content of the total injected dose was estimated following correction for geometry and transmission using a gamma camera. Cerebral blood flow was 579 +/- 163 ml/min (mean +/- SD) in Group A and 593 +/- 158 ml/min in Group B (p not significant (NS)). Myocardial flow in Group A was 266 +/- 82 ml/min and in Group B was 237 +/- 57 ml/min (p, NS). Total renal blood flow was 749 +/- 161 ml/min in Group A and 614 +/- 181 ml/min in Group B (p less than 0.01). There was a negative correlation between cardiac index and the percentage of the cardiac output distributed to brain (r = -0.70, p less than 0.01), heart (r = -0.67, p less than 0.01) and kidneys (r = -0.47), p less than 0.05). Low output cardiac failure is, therefore, associated with relative preservation of cerebral and myocardial blood flow and, to a lesser extent, of renal flow. A similar technique using dual labelling would allow an accurate estimation in individual patients, of the change in organ blood flow associated with transient alterations in cardiac output states.

Adult↗
PubMed1986

Prolonged metabolic recovery allows late identification of ischemia in the absence of electrocardiographic and perfusion changes in patients with exertional angina.

Regional myocardial perfusion and exogenous glucose uptake were assessed in 10 normal subjects and 10 patients with coronary artery disease and stable angina pectoris using 82Rubiduim and 18F-2-fluoro-2-deoxyglucose with positron emission tomography. At rest regional myocardial perfusion and glucose uptake in patients were comparable with those in normals. In 7 patients and 5 normals a supine bicycle exercise test was performed within the positron camera. In all 7 patients, exercise induced typical chest pain and ischemic electrocardiographic changes accompanied by regional abnormalities of myocardial perfusion which normalized 5 to 14 minutes after the end of exercise. In these patients 18F-2-fluoro-2-deoxyglucose was injected during recovery from exercise when all the parameters that were altered during the test, including myocardial perfusion, were back to control. In all 7, glucose uptake in the regions which showed abnormal perfusion during exercise was significantly higher than in the non ischemic regions (i.e. the ones with a normal increment of 82Rubidium uptake during exercise). In 2 patients the test was repeated on a different day and 18F-2-fluoro-2-deoxyglucose was injected during exercise in the presence of frank ischemia. In contrast to the injection following exercise, in both patients, glucose uptake in the ischemic region was found to be lower than in the non ischemic ones. In conclusion, in patients recovering from exercise-induced ischemia exogenous glucose utilization is enhanced in the previously ischemic myocardium. This occurs in the absence of symptoms and electrocardiographic changes and allows the identification and location of previous myocardial ischemia.

Angina Pectoris↗
PubMed1986

Clinical application of monitoring techniques: hemodynamic monitoring.

In the diagnosis of myocardial ischemia continuous hemodynamic monitoring may contribute to detection of transient ischemia, to definition of location and to elimination of its pathogenesis, and to characterization of hemodynamic response to ischemia. It can be helpful in investigating the significance of negligible, non specific and/or short-lasting electrocardiographic changes accompanying typical anginal symptoms. Simultaneous right ventricular and left ventricular pressure monitoring gives information regarding biventricular interaction during episodes of transient ischemia: an early left ventricular dysfunction, with or without a late right ventricular impairment, a selective right dysfunction, and a simultaneous left ventricular and right ventricular impairment all represent the hemodynamic patterns associated with left, right and biventricular ischemia respectively. Monitoring of hemodynamic parameters related to myocardial oxygen consumption and the study of their changes preceding the onset of ischemia during both spontaneous and provoked episodes of ischemia, may help in identifying whether functional or organic factors or both are involved in the pathogenesis of transient ischemia in individual patients. Two principal hemodynamic patterns appear to be associated with transient ischemia: a) left ventricular and/or right ventricular impairment, usually beginning shortly before the onset of electrocardiographic changes, followed by a rapid recovery and often an overshooting, b) a sudden and sustained increase in systolic pressure and heart rate, simultaneous with the onset of ST-T changes. In both cases, the 'excitatory' pattern appears to be unrelated to pain.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1986

Myocardial ischemia in man: current concepts, changing views and future investigation.

Over the past few years the focus of patient management has begun to extend from the mere detection and treatment of chronic coronary atherosclerotic obstructions to the attempt to understand, diagnose and treat the varied mechanisms responsible for acute myocardial ischemia. Management of patients with ischemic episodes is directed to: control of symptoms and/or signs of ischemia; improve prognosis. Several types of effective drugs are available but because of the incomplete knowledge of pathogenesis their use is still largely empirical. When medical therapy fails, surgery and angioplasty can improve coronary flow reserve considerably and even bring it back to normal. In contrast the goal of improving prognosis is more difficult to assess on an individual basis due to the heterogeneity of groups sufficiently large to ensure statistical analysis in long term follow-up and randomised studies. This makes it impossible to apply the average risk of a group to individual patients. For the future, major challenges remain: it will be necessary to learn more not only about the pathogenesis of coronary atherosclerosis but also about the vasomotor control of large and small coronary arteries, the local and systemic factors leading to coronary thrombosis, the myocardial and coronary response to ischemia, and the genesis of ischemic arrhythmias. Finally, since for the majority of coronary patients management is more often concerned with prognosis than with symptoms, we ought to know in more detail the natural history of the various forms of ischemic heart disease: if any given patient is to be allocated with reasonable precision to a prognostic group, the criteria used to categorize patients must be accurate and multiple.

Angina Pectoris↗
PubMed1985

Mixed angina pectoris.

Patients who present with episodes of angina caused both by an increase in oxygen demand and by transient impairment of supply have a mixed form of angina. Distinctive clinical features allow the classification of patients in everyday practice. At one end of the spectrum are patients who have angina only and always when they exercise beyond an essentially fixed level; their angina is fairly predictable and has been termed secondary angina. At the other end of the spectrum are patients who have a normal exercise tolerance but have angina at rest or during activities usually well tolerated that must be caused by a transient impairment of coronary blood flow; their angina is typically unpredictable and has been termed primary angina. We adopted the term primary to emphasize the possible existence of multiple causes of impairment of coronary flow, which together are to be contrasted with the traditional prevailing concept of angina being secondary to excessive increase in demand. In between these ends of the spectrum are most of the patients with angina pectoris encountered in clinical practice: they have a rather predictable ceiling of exercise that they cannot exceed without developing angina, but they also have a variable proportion of unpredictable anginal attacks that occur spontaneously or at levels of activity that are usually well tolerated. We introduced the concept of mixed forms of angina when we became aware that the same patient could experience angina both as a result of an excessive increase in myocardial demand, i.e., secondary angina, and as a result of the transient impairment of coronary blood flow supply, i.e., primary angina.

Angina Pectoris↗
PubMed1985

Mechanisms of ischemic cardiac pain and silent myocardial ischemia.

The mechanisms of cardiac ischemic pain remain obscure. It is unknown whether ischemia causes cardiac pain by the release of chemical substances or by mechanical stretching. It is also unknown whether ischemia activates specific nociceptors and pain fibers or mechanoreceptors and chemoreceptors. In patients who have both painful and painless ischemic episodes, a certain minimal duration and severity of ischemia are necessary but insufficient to explain the presence of pain, since very severe ischemia of long duration can be silent. Thus, central transmission of painful stimuli and the pain perception threshold appear to play major roles in determining the presence or absence of pain. The emotional state and psychologic expectations of patients may affect their perception and threshold of pain considerably.

Angina Pectoris↗
PubMed1985

Different susceptibility to myocardial ischemia provoked by hyperventilation and cold pressor test in exertional and variant angina pectoris.

Coronary constriction at the site of atherosclerotic stenoses has been suggested to play an important role in modulating the frequency of symptoms in patients with exertional angina. To investigate whether stimuli triggering coronary constriction have similar effects in patients with exertional and variant angina, responses to hyperventilation (HV) and cold pressor test (CPT) were evaluated. Twenty patients with chronic exertional angina, positive exercise test results and coronary heart disease were compared with 14 patients with variant angina and ST-segment elevation during an ergonovine test. In patients with exertional angina, the CPT produced diagnostic ST-segment depression in 6 of 20 patients (30%) at levels of rate-pressure product much lower than those during the exercise test; all patients had low effort tolerance and severe coronary artery disease. HV produced diagnostic ST-segment depression in only 1 of 20 patients (5%) (p less than 0.05 compared to that with CPT). Conversely, in patients with variant angina, HV produced ST-segment elevation in 11 of 14 patients (78%) and CPT produced elevation in only 2 of 14 (14%) (p less than 0.01). Thus, coronary constriction can provoke myocardial ischemia not only in patients with variant angina but also in some patients with exertional angina. Furthermore, the 2 groups of patients have a different susceptibility to stimuli known to produce coronary constriction.

Adult↗
PubMed1985

Efficacy of carvedilol (BM 14,190), a new beta-blocking drug with vasodilating properties, in exercise-induced ischemia.

The exercise response to a single oral dose (25 mg) of a new beta-blocking agent that also has potent vasodilating properties, carvedilol (BM 14,190), was assessed in 15 patients with stable exertional angina, positive exercise test responses (greater than or equal to 1 mm of ST depression) and coronary artery disease. A single-blind, placebo-controlled, randomized, crossover design was used. Compared with placebo, 25 mg of carvedilol significantly reduced both heart rate (HR) and blood pressure (BP) at rest (p less than 0.01). After administration of carvedilol, 10 of 15 patients did not have angina at peak exercise (p less than 0.01) and 5 had ST shifts of less than 1 mm (p less than 0.05). Total exercise time and time to 1 mm of ST depression were prolonged and ST-segment depression at peak exercise was significantly reduced (p less than 0.01). Systolic BP was reduced both at peak exercise and at 1 mm of ST depression (p less than 0.05), 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 (p less than 0.05). However, 4 patients actually achieved a higher HR-BP product but did not have angina and had less ST depression (or no ST-segment shifts) at peak 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 potent vasodilatory properties.

Adrenergic beta-Antagonists↗