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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 361 records · Page 20Linked to original sources
PubMed1984

Myocardial ischemia during ergonovine testing: different susceptibility to coronary vasoconstriction in patients with exertional and variant angina.

Coronary spasm is an accepted cause of transient myocardial ischemia in patients with variant angina; more recently it has been suggested that dynamic stenoses could also play an important role in the pathophysiology of exertional angina. To test this hypothesis we submitted 31 patients with histories typical of exertional angina to ergonovine testing and compared the electrocardiographic and clinical responses to those observed in seven patients with variant angina. All underwent bicycle ergometric exercise testing and coronary angiographic examination. For all tests, ST segment shifts of 0.1 mV or greater were considered to be diagnostic of myocardial ischemia. In patients with exertional angina, exercise testing produced diagnostic ST segment depression in 21 (68%). Ergonovine testing produced diagnostic ST segment depression in nine (29%). All nine had positive exercise test results and two- or three-vessel disease, yet the test was negative in seven other patients with positive exercise test results and similar angiographic findings. Conversely, in the seven patients with variant angina, results of exercise testing were positive in five (ST segment depression in two, ST elevation in three), while ergonovine produced ST segment elevation in all seven. Coronary angiographic examination showed normal arteries in two, one-vessel disease in four, and three-vessel disease in one. Results of all ergonovine tests were positive at values of rate pressure product much lower than those observed during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Ergonovine-induced myocardial ischemia: no role for serotonergic receptors?

Because ergonovine appears to produce coronary contractions by a serotonergic (5-HT) mechanism, we attempted to prevent ergonovine-induced ischemia in patients with vasospastic angina by pretreatment with ketanserin, a new selective 5-HT blocker. We studied seven patients with consistently positive results of ergonovine testing (ST segment elevation in three and ST segment depression in four). Ergonovine testing was performed before and after a bolus of 10 mg of ketanserin (all patients) and infusion of 2 to 4 mg/hr for 8 hr (six patients). To assess 5-HT blockade during ketanserin infusion, the constrictor response of hand veins to 5-HT was tested before and after ketanserin. Despite evidence of 5-HT blockade in hand veins, ergonovine-induced ischemia was not prevented by ketanserin in any patient, and there was no significant change in the dose of ergonovine required to provoke ischemia. In one patient, four spontaneous episodes of ST segment elevation occurred during infusion of ketanserin. The plasma concentrations of ketanserin at the time of ergonovine testing ranged from 61 to 127 ng/ml (mean 102) and were well above those that completely inhibit canine coronary 5-HT contractions in vitro. Although human coronary arteries may differ in their responsiveness to 5-HT or ketanserin, these data suggest that ischemia from ergonovine-induced coronary vasospasm is not mediated by 5-HT receptors.

Aged↗
PubMed1983

Myocardial ischaemia during daily life in patients with stable angina: its relation to symptoms and heart rate changes.

In thirty patients with stable angina and positive exercise tests, ambulatory ST segment monitoring was used to record episodes of transient myocardial ischaemia during daily life. All patients had four consecutive days of monitoring and in 20 patients long-term variability was assessed by repeated 48 hour monitoring and exercise testing over 18 months. There were 1934 episodes of rectilinear or downsloping ST-depression (911, 1 mm; 638, 2 mm; 385, greater than 3 mm) in 446 days of recording, of which only 470 (24%) were accompanied by angina. Positron tomography showed evidence of regional myocardial ischaemia during both symptomatic and asymptomatic ST depression. On average, heart rate at the onset of both symptomatic and asymptomatic ST episodes was significantly lower than the rate at the onset of ST depression during exercise testing (98 +/- 20.5 vs 124 +/- 17 beats/minute). Heart rate rose by more than 10 beats in the minute preceding ST depression in only 23% of episodes. Over 18 months, 8 (40%) patients exhibited marked variability in the number of daily ST episodes. Variability of ST depression was consistently underestimated by symptoms and not reflected by exercise testing. Thus, patients with stable angina showed frequent, variable, and often asymptomatic electrocardiographic evidence of ischaemia. Heart rate increase was not common before myocardial ischaemia, suggesting that, in such patients, transient impairment in coronary supply may be at least as important as excessive increase in demand in the genesis of ischaemia during daily life.

Activities of Daily Living↗
PubMed1983

Variable susceptibility to dynamic coronary obstruction: an elusive link between coronary atherosclerosis and angina pectoris.

Growing evidence suggests that dynamic coronary obstructions play an important but elusive role in the genesis of ischemic events. Dynamic coronary obstructions can develop during certain phases of coronary disease as a result of a variable combination of vasoconstriction, arterial wall lesions, and increased thrombotic tendency. In a certain phase of their disease some patients develop dynamic coronary obstruction, while others with a similar degree of fixed atherosclerotic obstruction do not.

Angina Pectoris↗
PubMed1983

Safety and effectiveness of a portable external automatic defibrillator-pacemaker.

Sudden cardiac death in the community can be reduced by early resuscitation. The commonest arrhythmia encountered in this setting is ventricular fibrillation. A portable external automatic defibrillator-pacing machine for use by emergency services and laymen after basic training, has recently been introduced. This device has a tongue-abdominal pathway for sensing the electrocardiogram and respiration, as well as delivery of current. In its automatic mode, the machine cannot defibrillate unless the patient's breathing and gag reflex are virtually absent. The decision-making characteristics of the machine were defined in isolation from the patient using simulated ECG signals and recordings of arrhythmias obtained during cardiac surgery and during electrophysiological studies. The pathway was evaluated separately by attaching it to a conventional defibrillator and using it in the elective cardioversion of 15 patients. Electrode sites were examined and creatine phosphokinase (CPK) and creatinine phosphokinase isoenzyme (CPKMB) release determined following conversion. Repeated playback of the same 34 minutes of selected recordings showed that decisions were consistent 95% of the time. Automatic pacing always occurred with asystole. ECG signals less than 0.35 mV in amplitude were not recognized, but a manual override switch could be operated in those circumstances where there was failure to act upon fine ventricular fibrillation. Defibrillation of 50% of the recordings of supraventricular and ventricular tachycardia did occur, but this could not have happened in practice unless the patient was unconscious, and in addition, the operator failed to countermand this decision. The tongue-abdominal pathway yielded good recordings of the ECG.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗
PubMed1983

Computed tomography of the heart: initial experience.

Computed tomography (CT) provides non-invasive diagnosis of cardiac lesions by direct demonstration of the myocardium and the individual cavities of the heart. The potential role of CT scanning in the detection and quantitation of acute myocardial infarction has been previously investigated in experimental animals. Initial experience in assessing 10 patients admitted with recent infarction on biochemical and electrocardiographic evidence is reported. Intravenous infusion of iodinated contrast agents produced contrast enhancement either of the rim or diffusely through the myocardium in the area of infarct, as sited electrocardiographically. Patients with coronary artery bypass grafts and hypertrophic cardiomyopathy have also been studied by this method. Cardiac CT with intravenous administration of contrast may have an important role in the future in assessment and follow-up of ischaemic heart disease.

Cardiomyopathy, Hypertrophic↗
PubMed1983

Impairment of myocardial perfusion and function during painless myocardial ischemia.

Left ventricular (or pulmonary and systemic arterial) hemodynamics were measured for a mean of 13.6 hours during continuous electrocardiographic monitoring in 14 patients admitted to the coronary care unit because of angina at rest. Of 293 episodes of transient ST segment and T wave changes identified, 247 (84%) were completely asymptomatic. Sixty-three percent of asymptomatic episodes were associated with an elevation of the left ventricular end-diastolic or pulmonary artery diastolic pressure of 5 mm Hg or more; in 15% there were smaller elevations (2 to 4 mm Hg) and in 22% there were no changes or less than a 2 mm Hg elevation of pressure. The peak contraction and relaxation dP/dt (first derivative of left ventricular pressure) were reduced to 100 mm Hg/s or more in 84 and 81% of asymptomatic episodes, respectively. Great cardiac vein oxygen saturation measured in three patients showed an increased myocardial oxygen extraction similar to that seen in painful episodes, which preceded and accompanied asymptomatic electrocardiographic changes. These results indicate that asymptomatic electrocardiographic changes represent transient myocardial ischemia. Comparison of asymptomatic and symptomatic episodes revealed that asymptomatic episodes were generally shorter (253 +/- 159 versus 674 +/- 396 seconds, probability [p] less than 0.001) and produced less impairment of left ventricular function: there were smaller elevations of left ventricular end-diastolic or pulmonary artery diastolic pressure (5.9 +/- 5.0 versus 16.5 +/- 6.9 mm Hg, p less than 0.001), and smaller reductions of peak left ventricular contraction dP/dt (252 +/- 156 versus 395 +/- 199 mm Hg/s, p less than 0.001) and relaxation dP/dt (259 +/- 191 versus 413 +/- 209 mm Hg/s, p less than 0.001). In individual patients, however, asymptomatic and symptomatic episodes of similar duration and severity were observed. The duration and severity of ischemia appear important for the genesis of anginal pain, but additional factors must be involved.

Adult↗
PubMed1983

Regional extravascular lung density and fractional pulmonary blood volume in patients with chronic pulmonary venous hypertension.

Using a technique based on positron transmission and emission tomography, we measured regional extravascular lung density (lung tissue and interstitial water per unit thoracic volume) and fractional pulmonary blood volume (volume of blood per unit thoracic volume) in normal subjects and in patients with cardiomyopathy and chronic pulmonary venous hypertension. We found an increase in extravascular lung density in the patients. Extravascular density was increased in all parts of the lung studied, but higher values were seen in the dorsocaudal portion than in the ventrocaudal portion of the lung (average 151% and 130% of normal, respectively). Fractional blood volume was markedly reduced in the dorsocaudal part of the lung (mean 74% of normal). The increase in extravascular density probably reflects structural changes in the lung as well as accumulation of interstitial fluid. The distribution of extravascular density is consistent with previous radiological and morphological studies, and may reflect a higher tendency to oedema formation in the dependent parts of the lung. The measurements of fractional blood volume suggest that intrapulmonary blood volume is reduced in chronic pulmonary venous hypertension. This may reflect a decrease in the distensibility of the pulmonary vessels due to structural abnormalities, as well as functional changes in the pulmonary vasculature.

Adult↗
PubMed1983

Intravenous dl-carnitine fails to increase the double-product during atrial pacing in patients with effort angina. A double-blind randomized study.

Infusions of DL-carnitine are reported to improve the tolerance to atrial pacing of patients with angina pectoris. In the present study, six patients with angina of effort and triple vessel disease received two placebo and two carnitine infusions administered in a double-blind randomized fashion. Carnitine did not affect either the double product (heart rate X systolic blood pressure) at maximal pacing (ST depression: 2.3 +/- 0.2 mm, +/- SEM) or the tolerated pacing time. Intravenous carnitine, in the dose given, is of no therapeutic benefit in myocardial ischemia precipitated by tachycardia. It could be effective when free fatty acids are elevated as during catecholamine stimulation.

Angina Pectoris↗
PubMed1982

Vasospastic ischemic mechanism of frequent asymptomatic transient ST-T changes during continuous electrocardiographic monitoring in selected unstable angina patients.

Asymptomatic episodes of ST segment and/or T wave changes are often reported during Holter monitoring in patients with angina pectoris. However, the interpretation of such changes is debated relative to silent myocardial ischemia. We studied 11 patients admitted to the CCU because of frequent episodes of unstable anginal attacks who had undergone repeated periods of Holter monitoring, characterized by predominantly occurring asymptomatic episodes of ST segment and/or T wave changes associated with less frequent typical anginal attacks. In a total of 89 days of Holter monitoring, the patients evidenced 520 episodes of transient ECG changes including 180 of ST elevation, 73 of ST depression, and 267 of T wave alterations. Only 12% of episodes were symptomatic. Coronary injection during asymptomatic ST-T changes was performed in eight patients. In six it was possible to document spontaneous coronary spasm. In seven patients ergonovine administration induced anginal pain, ST-T changes, and coronary spasm. In all patients the anginal attacks completely disappeared with medical treatment and the asymptomatic episodes were abolished in six and reduced in four. Our findings support the hypothesis that in certain selected unstable anginal patients, transient asymptomatic ECG changes are caused by acute myocardial ischemia.

Angina Pectoris↗
PubMed1982

Role of coronary arterial spasm in sudden coronary ischemic death.

Sudden coronary death is a syndrome caused by different mechanisms, all of which should be separately considered with respect to preventive measures. Ventricular fibrillation, tachycardia, and complete atrioventricular block were repeatedly observed during ischemic episodes caused by spasm in both the presence and absence of anginal pain. Spasm is, therefore, a potential cause of sudden coronary death. In "variant" angina, which is a reasonably reliable indicator of coronary spasm, arrhythmias occur in about 25% of patients and tend to recur in the same patient. The severity of coronary atherosclerosis in patients who develop severe arrhythmias is quite variable and not dissimilar from patient who do not. Mortality is considerably higher in patients with severe disease, but fibrillation and death can occur also in patients with angiographically normal arteries. In these patients acute and long-term treatment with nitrates and slow channel blockers appears to give remarkable results. Prevention of arrhythmias in patients in whom arrhythmias are secondary to acute ischemic episodes caused by vasospasm should be attempted by preventing vasospasm.

Arrhythmias, Cardiac↗
PubMed1982

Measurement of serum C-reactive protein concentration in myocardial ischaemia and infarction.

Serum C-reactive protein (CRP) and creatine kinase (CK) MB levels were measured prospectively in patients with definite myocardial infarction, patients with spontaneous or exercise-induced angina, subjects undergoing coronary arteriography, and patients with non-cardiac chest pain. All individuals with infarction developed raised CRP levels and there was a significant correlation between the peak CRP and CK MB values. The CRP, however, peaked around 50 hours after the onset of pain at a time when the CK MB, which peaked after about 15 hours, had already returned to normal. In 20 patients who recovered uneventfully, CRP levels fell, returning to normal about seven days after infarction in four cases who were followed to this point. In eight complicated cases, including four who died within the first 10 days, the CRP level remained high. Angina alone or coronary arteriography did not cause a rise in the CRP or CK MB concentrations. Increased CRP production is a non-specific response to tissue injury and raised CRP levels in cases of chest pain with a normal CK MB indicated a pathological process other than myocardial infarction. Regular monitoring of CRP levels may also assist in early recognition of intercurrent complications occurring after myocardial infarction.

Angina Pectoris↗
PubMed1982

Effects of intravenous prostacyclin in variant angina.

A lack in prostacyclin (PGI2) production due to atherosclerosis may play a role in the pathophysiology of some of the clinical manifestations of ischemic heart disease and in particular, of coronary vasospasm. We therefore evaluated the effects of i.v. PGI2 in nine patients with variant angina and six normal volunteers. In normal subjects, PGI2 (2.5, 5, 10 and 20 micrograms/kg/min) had significant antiplatelet effects, caused a dose-dependent decrease in both systolic and diastolic arterial pressure and a decrease in pulmonary resistance. Heart rate increased in a dose-dependent manner, but no consistent effects on myocardial contractility (evaluated by ultrasound) were observed. Side effects were negligible and readily reversible. Although producing obvious antiplatelet and vasodilatory effects, PGI2 did not affect the number, severity and duration of spontaneous ischemic episodes due to coronary vasospasm in five patients and ergonovine-induced spasm in three. However, the number of ischemic episodes was consistently reduced in one patient during four consecutive periods of PGI2 infusion alternated with placebo. a severe, prolonged ischemic episode with ST elevation and pain was consistently observed in this patient every time PGI2 was discontinued. In the appropriate environment, PGI2 can be administered safely to patients with ischemic heart disease. Occasionally, PGI2 may result in a complete disappearance of ischemic episodes due to coronary vasospasm, but usually it is ineffective. These conflicting results could be related to different etiologies of coronary spasm.

Adult↗
PubMed1982

Failure of thromboxane A2 blockade to prevent attacks of vasospastic angina.

Thromboxane A2 (TxA2), released by aggregating platelets, has been proposed as a potential mediator of coronary vasospasm. We studied six patients with variant angina, a clinical syndrome due to coronary vasospasm, and one patient with frequent recurrent episodes of transient ST-segment depression at rest in whom the spasm was demonstrated angiographically. All patients underwent continuous ECG monitoring for 2 days before and 2 days after a single, low, i.v. dose of aspirin (2 mg/kg), which reduced TxB2 (the stable metabolite of TxA2) to less than 3% of the control values. There were 129 transient ischemic episodes during control and 146 after aspirin, when platelet TxB2 was reduced to negligible levels. The duration, severity and incidence of symptomatic episodes were not significantly affected by TxA2 blockade. We conclude that platelet TxA2 is probably not responsible for the initiation of coronary vasospasm.

Adult↗