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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 289 records · Page 16Linked to original sources
PubMed1989

Substance P dilates epicardial coronary arteries and increases coronary blood flow in humans.

The effects of intracoronary infusions of substance P in conscious humans on epicardial vessel diameter and coronary sinus oxygen saturation were investigated in 13 patients who had angiographically normal coronary arteries. The dose of substance P ranged from 2.8 to 89.6 pmol/min, starting at 2.8 pmol/min and rising by doubling increments. All infusions were performed for 2-minute periods. Epicardial vessel diameter was measured by a computerized analysis system (CAAS) of the angiogram performed at the end of each infusion period. Coronary sinus oxygen saturation (CSO2) was measured continuously by a fiber-optic oximeter catheter in the coronary sinus. A reduction of arterial pressure, indicative of a systemic effect of substance P, occurred only when infusions were 44.8 pmol/min or more. At considerably smaller dosages, a dose-dependent increase in the left anterior descending artery diameter was seen with substance P; maximal dilation occurred at a dosage of 11.2 pmol/min. The percent increase in vessel diameter for this dosage was 29.4 +/- 19.8% (mean +/- SD) at the distal site of analysis and 16.7 +/- 10% at the proximal site of analysis. CSO2 rose in a dose-dependent manner and was maximal at a dosage of 11.2 pmol/min, which caused a 14.6 +/- 7.2% O2 rise above the preinfusion saturation of 43.5 +/- 11.1% O2. As the heart rate-blood pressure double product showed no change, it is argued that these changes in CSO2 probably reflect rises in coronary flow that were seen with dosages of substance P without systemic effect. In three patients, preconstriction induced by ergonovine was reversed by substance P infusions, which produced a degree of dilation equivalent to that of isosorbide dinitrate. We conclude that substance P at very small dosages, which are without peripheral effects, causes in vivo epicardial coronary artery dilatation as well as resistive vessel dilatation in humans.

Adult↗
PubMed1988

Mean platelet volume and size distribution and their sensitivity to agonists in patients with coronary artery disease and congestive heart failure.

Mean platelet volume was related to platelet count in patients with myocardial infarction (n = 55) and patients with congestive heart failure (n = 9). 18 patients with acute myocardial infarction were tested at admission and 4-7 days later, together with 13 patients with chronic stable angina and 10 patients with chest pain which was not related to coronary artery disease. In citrated blood a relative reduced frequency of large platelets (greater than 13 fl) occurred in patients with acute myocardial infarction at admission but was not seen during recovery or in patients with chronic stable angina. This suggests consumption of large platelets at time of thrombus formation. No relation was found between plasma catecholamine levels and mean platelet volumes. Effects of serotonine, adrenaline and CGP 28392, a calcium agonist, on platelet volume distributions were determined. Sensitivity of platelets to adrenaline was increased in patients with acute myocardial infarction on admission and reduced 4-7 days later, while in patients with congestive heart failure reactivity to both serotonine and adrenaline were reduced. This indicates a fast down-regulation during the early recovery phase of myocardial infarction and chronically in congestive heart failure.

Adult↗
PubMed1988

Abnormalities in myocardial metabolism in patients with unstable angina as assessed by positron emission tomography.

Regional myocardial perfusion and glucose metabolism were assessed in six normal volunteers and 29 patients with coronary heart disease and stable or unstable angina using rubidium-82 (Rb-82) and F-18 fluoro 2-deoxy-D-glucose (FDG) with positron emission tomography. All normals and patients were studied following overnight fasting, at rest, with no angina or electrocardiographic signs of acute myocardial ischemia or necrosis. Rb-82 myocardial cross-sectional images were obtained employing the continuous infusion technique, while dynamic FDG imaging was employed after intravenous tracer bolus injection. Regional Rb-82 and FDG myocardial concentrations were then calculated by drawing regions of interest over the interventricular septum, anterior and lateral wall of the left ventricle. The mean Rb-82 uptake for each left ventricular region analyzed was found to be similar between both groups of patients and normal volunteers. The mean myocardial glucose utilization was found to be similar in normal volunteers and patients with stable angina (0.023 +/- 0.032 vs. 0.012 +/- 0.008 microns ml/min p less than 0.42). However, myocardial glucose utilization was found to be significantly higher in patients with unstable angina compared with both normals and patients with stable angina (0.048 +/- 0.047 microM/ml/min p less than 0.001 for both comparisons). Thus, in patients with severe coronary artery disease and unstable angina, myocardial glucose utilization was enhanced in spite of the absence of clinical, electrocardiographic, or detectable perfusion evidence of acute ischemia.

Adult↗
PubMed1988

Coronary constriction in acute myocardial infarction: role of nitrates.

We have investigated the coronary vasodilator responses to nitrates in the early stages of acute myocardial infarction before, during and after the administration of thrombolytic therapy. Before thrombolysis, intracoronary doses (2-4 mg) of isosorbide dinitrate failed to induce recanalisation of the totally occluded infarct related artery. Episodes of coronary reopening and reocclusion associated with ST-segment resolution and re-elevation were frequently observed both spontaneously before and during thrombolytic therapy. In 50-86% of patients, intracoronary isosorbide dinitrate promptly re-established full coronary patency immediately after acute reocclusion or whenever coronary occlusion was incomplete, both before and during thrombolysis. After thrombolysis further intracoronary isosorbide dinitrate dilated the infarct related stenoses but not uninvolved adjacent normal coronary branches. Coronary thrombosis and constriction frequently interact during the early phases of acute myocardial infarction. The combination of high local concentrations of nitrates with thrombolytic agents promotes stable coronary recanalization and may be beneficial in patients with acute myocardial infarction.

Coronary Vessels↗
PubMed1988

Adenosine-induced chest pain in patients with silent and painful myocardial ischaemia: another clue to the importance of generalized defective perception of painful stimuli as a cause of silent ischaemia.

Adenosine is formed from adenosine triphosphate within the ischaemic cells from where it is released into the coronary circulation. Adenosine exhibits several cardiovascular effects which tend to protect the ischaemic myocardium. Based on the observation that in healthy volunteers the intravenous infusion of adenosine produces angina-like chest pain, it has been recently proposed that another cardioprotective action of this substance could be provocation of angina. If this is the case adenosine should not produce chest pain in patients with silent ischaemia. To test this hypothesis we infused this substance intravenously at increasing doses of 50, 100, 150, 200, 250 and 300 micrograms kg-1 min-1 in eight patients with silent ischaemia (group A). All of them developed ST depression (1.8 +/- 0.2 mm) during exercise testing and seven also during adenosine infusion (1.1 +/- 0.8 mm). However, none of the patients had chest pain during exercise while seven had chest pain during adenosine. We then infused adenosine in eight other patients (Group B) who had painful ischaemia and an exercise tolerance similar to that of Group A patients (time to 1 mm ST depression 8.6 +/- 2.7 min and 8.4 +/- 3 min, respectively, P = NS). Adenosine induced chest pain in all Group B patients. The time to pain onset during adenosine was similar in the two groups (9.3 +/- 2.3 min in Group B and 12.4 +/- 4.9 min in Group A).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1988

Pre-existing coronary stenoses in patients with first myocardial infarction are not necessarily severe.

The sudden, often unheralded, onset of symptoms in acute myocardial infarction suggests that pre-existing coronary stenoses susceptible to acute thrombosis in the infarct-related artery may not necessarily have been severe. We investigated the severity of residual coronary stenoses after successful thrombolytic recanalization and the relationship to previous symptoms, collateral vessels and the extent of coronary artery disease in 60 consecutive patients at the time of presentation of their first acute myocardial infarction by performing quantitative coronary arteriography before, during and after intracoronary thrombolytic therapy. Recanalization was achieved in 48 (80%) patients with a residual stenosis of 58.1 +/- 10.8% (mean +/- ISD; range 33-82%) obstruction diameter and a minimum lumen calibre of 1.10 +/- 0.3 mm (range 0.39-1.95 mm). A residual stenosis of less than 60% obstruction diameter was present in 28 (47%) patients. When residual stenoses were mild, no acute collateral filling of the occluded artery was observed. After thrombolysis, residual infarct-related coronary stenoses in patients with their first acute myocardial infarction are not necessarily severely obstructive. This raises the problem of identifying which non-obstructive coronary stenoses are likely to occlude suddenly and why they do so.

Adult↗
PubMed1988

Laser recanalisation of coronary arteries by metal-capped optical fibres: early clinical experience in patients with stable angina pectoris.

The delivery of laser energy to the coronary circulation by bare optical fibres may cause perforation of the vessel. Experimental studies have shown that this complication can be avoided if the optical fibre is fitted with a metal cap to prevent the potentially dangerous forward projection of the laser beam. This study was performed to assess the feasibility and short term effects of percutaneous coronary laser recanalisation with these modified fibres. Recanalisation of a severe stenosis of the left anterior descending artery was attempted in six patients who were referred for coronary artery bypass grafting. Although the percutaneous technique was used, the laser procedure was performed during coronary bypass surgery before the start of cardiopulmonary bypass to minimise the effects of potential complications. A 1.5 mm diameter metal-capped fibre coupled to an argon laser was advanced percutaneously over a guide wire positioned across the stenosis. In the first patient the delivery of 152 J resulted in the gradual passage of the fibre through a 3 cm long stenosis. Repeat angiography showed a reduction in the severity of the stenosis. In the second patient the delivery of 112 J failed to allow fibre advancement; a further 80 J pulse caused perforation which was repaired. In the remaining four patients the delivery of laser energy in the attempt to traverse the stenosis was limited to less than 90 J. In two of the four patients the severity of stenosis was reduced. No further complications were seen. Percutaneous coronary laser recanalisation with metal-capped optical fibres is feasible but improvements of currently available technology are needed to increase the primary success rate.

Aged↗
PubMed1988

Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia.

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium-99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The maximum increase in end-diastolic volume was slightly greater in painful than in painless episodes, 38 +/- 8.0% versus 28 +/- 12.4%, but no significant difference was observed in the rate of volume change or in the maximum increase of end-systolic volume (133 +/- 50% and 110 +/- 27.3%), stroke volume (-28 +/- 15% and -25 +/- 12.4%), or ejection fraction (-32 +/- 8.7% and -26 +/- 6.0%). Although the maximum end-diastolic volume achieved is greater in painful episodes, this effect cannot be separated from that of duration, and, furthermore, there was no significant difference in end-diastolic volume at the moment chest pain began. Thus, in patients with angina at rest, transient asymptomatic ST segment shifts are consistently associated with large changes in left ventricular volume, similar to those observed during painful episodes. The rate and extent of acute left ventricular dilatation do not appear to be factors directly causing anginal pain.

Angina Pectoris↗
PubMed1987

Beneficial effect of nitrates on myocardial glucose utilization in unstable angina pectoris.

Myocardial uptake of the glucose analog F-18-2-fluoro-2-deoxy-D-glucose (FDG) was assessed by positron emission tomography in 6 normal volunteers, 7 patients with chronic stable angina and 22 patients with unstable angina at rest in fasting conditions. Regional myocardial perfusion was assessed by rubidium-82. The study was repeated a few days later after intravenous infusion of isosorbide dinitrate. FDG uptake was similar in control subjects and patients with stable angina (0.023 +/- 0.032 vs 0.012 +/- 0.008 mol/ml/min, p less than 0.42) but was about 4-fold higher on the average in patients with unstable angina (0.084 +/- 0.047, p less than 0.01). The severity of coronary obstructions in stable and unstable angina patients was similar. The increased uptake involved the whole heart, including areas not distal to critically stenosed vessels; it was not associated with reduced myocardial perfusion and was not related to a recent episode of transient ischemia as assessed by symptoms and by Holter monitoring. After continuous infusion of nitrates, FDG uptake was consistently and significantly reduced toward normal levels both in areas perfused by critically stenosed coronary arteries and by noncritically stenosed vessels.

Adult↗
PubMed1987

Intermittent coronary occlusion in acute myocardial infarction. Value of combined thrombolytic and vasodilator therapy.

We performed continuous electrocardiographic ST-segment monitoring and serial coronary arteriography in 45 consecutive patients presenting in the early stages of acute myocardial infarction. During cardiac catheterization, 28 episodes of arteriographically confirmed coronary reopening and subsequent reocclusion were observed in 16 patients before (3 episodes) and during (25 episodes) continuous intracoronary infusion of streptokinase. In addition, ST-segment monitoring demonstrated 12 episodes of spontaneous transient return of the ST segment to the base line in eight patients between the time of admission and the performance of coronary arteriography. During arteriographically documented reocclusion, intracoronary isosorbide dinitrate (2 mg) reestablished the patency of the coronary artery within one to two minutes in 14 of 28 episodes that occurred in 11 of 16 patients. After streptokinase infusion, intracoronary administration of isosorbide dinitrate was followed by dilatation of the infarct-related stenosis from a mean value (+/- SD) of 1.12 +/- 0.3 mm (58.1 +/- 12.1 percent) to 1.33 +/- 0.4 mm (51.6 +/- 12.9 percent; P = 0.004). Spontaneous intermittent coronary recanalization and reocclusion resulting from a variable combination of thrombosis and vasoconstriction are frequent during the early phase of acute myocardial infarction. We propose that the combination of intracoronary streptokinase and isosorbide dinitrate may increase the rate of stable coronary recanalization.

Adult↗
PubMed1987

Pain threshold and tolerance in women with syndrome X and women with stable angina pectoris.

A recent report showed that during Holter monitoring of patients with syndrome X (typical anginal pain, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries), 50% of episodes of ischemic ST-segment depression were painful. This proportion is considerably higher than that in patients with chronic stable angina, which is about 30%. A significantly lower threshold and tolerance to painful stimuli was seen in a group of patients with chronic stable angina in whom 50% of episodes were painful compared with a group in whom only 5% of episodes were silent. Hence, patients with syndrome X may have enhanced sensitivity to painful stimuli. To investigate whether this difference was due to a lower threshold for painful stimuli in general, 12 patients with syndrome X and 10 (age- and sex-matched) with chronic stable angina were studied using the same battery of painful stimuli. Patients with syndrome X had a significantly lower threshold and tolerance for forearm ischemia (-36%, p less than 0.05, and -40%, p less than 0.001) and electrical skin stimulation (-37%, p less than 0.01, and -35%, p less than 0.001); the cold pressor test did not show significant differences (-7%, p = 0.391, and -1%, p = 0.818). Thus, patients with syndrome X in this study had significantly lower threshold and tolerance values for forearm ischemia and for electrical skin stimulation. These differences in sensitivity to pain may partly explain a higher incidence of painful ischemic episodes detected by ambulatory electrocardiographic monitoring during unrestricted daily life.

Angina Pectoris↗
PubMed1987

Relative roles of preload increase and coronary constriction in ergonovine-induced myocardial ischemia in stable angina pectoris.

To assess the relative role of increased ventricular preload and critical coronary lesions in ergonovine-induced myocardial ischemia, 9 normal subjects (group A), 7 patients with stable angina (group B) and 5 with variant angina (group C) were studied. In all patients, the 12-lead electrocardiogram, blood pressure and left ventricular (LV) volume (technetium-99m blood pool) were continuously recorded before and during administration of incremental doses of ergonovine given at 5-minute intervals. In all subjects, an initial LV dilatation developed; in group B and C patients, this was followed by a decrease in stroke volume and ejection fraction with subsequent onset of electrocardiographic changes and angina. The interval between these events was significantly shorter in group C and in 3 group B patients; in these patients, signs of ischemia appeared with smaller ergonovine doses and at minimal preload increase, coronary constriction being the likely mechanism of ischemia. In the remaining 4 group B patients, the onset of stroke volume, ejection fraction, electrocardiographic changes and angina was significantly delayed, occurring after administration of larger ergonovine doses when LV volume was already considerably increased. This finding suggests that the loading effect of ergonovine on LV volume, rather than on coronary constriction, could be the prevailing mechanism of ergonovine-induced ischemia in these patients.

Angina Pectoris↗