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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hemodynamic, coronary sinus blood flow and myocardial metabolic effects of 0.15 mg/kg body weight of intravenously administered propranolol were studied in 19 patients with coronary artery disease and 6 normal patients. Atrial pacing was performed in all patients and produced angina in 15 of the 19 patients with coronary artery disease. In these patients propranolol reduced heart rate from 78 to 69 beats/min, cardiac index from 3.0 to 2.6 liters/min per m2 and left ventricular stroke work index from 47 to 43 g-m/m2; it increased total peripheral resistance from 24 to 28 units and lactate extraction from 16.3 to 22.5%. There was no significant change in mean arterial pressure, left ventricular end-diastolic pressure, coronary sinus blood flow or myocardial oxygen consumption. During a second pacing stress propranolol produced clinical improvement in 9 of the 15 patients who experienced angina initially. The improvement was associated with less severe abnormalities in S-T depression and left ventricular end-diastolic pressure, increased lactate extraction and no significant change in coronary sinus blood flow or myocardial oxygen consumption. Thus, propranolol appears to be capable of modifying the anginal threshold as determined with atrial pacing, and the clinical response appears to be independent of global changes in coronary sinus blood flow and myocardial oxygen consumption.
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PMID:Effects of propranolol on the hemodynamic, coronary sinus blood flow and myocardial metabolic response to atrial pacing. 87 19

Eighteen men with myocardial infarction in their history and without signs of heart failure were investigated at rest and during standard supine exercise. In nine patients aneurysma or diskinesis of the left ventricular wall were found. The left ventricular end-diastolic volume was determined from the wash-out of 133Xe injected into the left ventricle by means of precordial scintillation counting. During exercise the cardiac index rose owing to acceleration of the heart rate, whereas the stroke index remained unchanged, and the left ventricular work and stroke indices increased. The left ventricular end-diastolic pressure, elevated at rest, reached high values during exercise. The left ventricular end-diastolic and residual volumes decreased during exercise in most patients, and simultaneously the systolic ejection fraction increased. In patients with aneurysma or diskinesis the end-diastolic volume both at rest and during exercise does not differ from EDV of other patients. Six patients developed angina pectoris during exercise, but their haemodynamics did not differ significantly. It is concluded that the left ventricle in patients with advanced coronary heart disease and previous myocardial infarction shows the signs rather of diminished compliance than of heart failure during adequate exercise and still possesses some functional reserves.
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PMID:Left ventricular end-diastolic volume during supine exercise in patients with healed myocardial infarction. 90 91

Ten patients with angina pectoris underwent multistage maximal treadmill exercise with hemodynamic measurements before, and again 6 months following coronary artery surgery. Subjectively, 9 patients experienced a total and one patient partial relief from angina, and all patients noted improved exercise tolerance following surgery. Objectively, significant improvement was found in duration of exercise, maximal oxygen intake in maximal cardiac output, maximal heart rate, and maximal pressure-rate product. Surgery did not significantly affect systemic or pulmonary arterial pressures during exercise. Despite these improvements, maximal cardiac output did not return to normal levels following surgery, due to an unexpected but significant reduction in stroke volume.
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PMID:Maximal cardiac output in angina patients before abd after coronary artery surgery. 93 26

Fifty-three men with significant obliterative arteriosclerosis of coronary arteries were examined at rest, during and after pacing. Pacing induced both angina pectoris and depression of the ST segment in 38% of the patients; either angina pectoris or depression of ST segment, in 32% of the patients; the remaining 30% of patients were without symptoms or ECG signs of coronary insufficiency. Haemodynamic findings at rest, or during and after cessation of pacing were not different between these groups. Pacing increased heart rate, cardiac index remained unchanged, the stroke volume decreased, the left ventricular ejection time shortened. In both systemic and pulmonary arteries the systolic pressures decreased, the diastolic and mean pressures rose. The left ventricular end-diastolic pressure decreased. In 28 of the patients the myocardial metabolism was investigated. A close correlation was found between positive symptoms and ECG signs of myocardial ischaemia on the one hand, and metabolic signs on the other hand. Absence of angina pectoris and depressions of the ST segment during pacing does not exclude the presence of metabolic signs of ischaemia; an opposite finding is about three times less frequent. The study offers objective information about haemodynamics and myocardial metabolism before, during and after pacing, and represents an attempt of a simple classification of symptoms and signs of induced ischaemia.
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PMID:Haemodynamics and myocardial metabolism in patients with obliterative coronary arteriosclerosis and tachycardia induced by pacing. 100 Sep 81

Intraoperative haemodynamics was studied in 31 patients with pre-infarction angina pectoris and in 3 patients with acute myocardial infarction. Twelve of them (3 with myocardial infarction) were subjected to a graphic examination of 12 haemodynamic parameters. Aorto-coronary bypass procedures using autovenous grafts were demonstrated to improve the contractile function of the left-ventricular myocardium in this group of patients, as manifested in a decrease of the binite diastolic pressure, increase of the cardiac index and stroke volume in the aorta. Tracing the intraoperative haemodynamics helps in determining the immediate postoperative prognosis and in choosing the optimum regimens of drug therapy. The determination of the volume blood flow in the bypass with the help of a flowmeter is a compulsory procedure, since it permits an objective assessment of the adequacy of the conducted revascularization of the myocardium.
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PMID:[Intraoperative hemodynamics in patients with pre-infarct stenocardia and acute myocardial infarct]. 107 92

Left ventricular function was studied in 17 patients with ischaemic heart disease and compared with 4 patients with normal left ventricular function. The patients in the homogeneous group of ischaemic heart disease were further subdivided into those 'without angina' (n=5) and those 'with angina' (n=12), depending upon the presence of angina during supine leg exercise at the time of definitive study. At rest there was no significant difference in the heart rate, cardiac output, stroke volume, and left ventricular end-diastolic pressure (LVEDP) in the three groups. During exercise the cardiac output and stroke volume were significantly depressed and LVEDP was significantly raised in the ischaemic heart disease group as a whole but within this group failed to show any significant difference in patients with and without angina. The left ventricular end-diastolic volume (LVEDV) and end-systolic volume (LVESV) measurements showed clear separation of these three groups only on exercise. On exercise, there was decrease in LVEDV and LVESV (P less than 0.05; P less than 0.02) in the group with normal left ventricular function, no change in the group with ischaemic heart disease without angina, and striking increase in LVEDV and LVESV in the group with ischaemic heart disease and angina (P less than 0.01 and P less than 0.02, respectively). This angiographic method of assessing left ventricular function shows clear separation of the three groups and also highlights the significance of angina. Ejection fraction (EF), a commonly measured parameter of left ventricular function, failed to reflect consistent changes on exercise as compared to values at rest which emphasizes the limitations of the measurement of ejection fraction at rest.
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PMID:Left ventricular angiography on exercise. A new method of assessing left ventricular function in ischaemic heart disease. 108 66

The left ventricular haemodynamic alterations during right atrial pacing were studied in 12 cases. Cardiac index varied little: during maximal rate however, its mean value was slightly lower than the resting one. Stroke index decreased inversely to the heart rate. The course of these indices did not separate the normal from abnormal cases. Ventricular function curves (VFCs) were constructed by relating the changes of left ventricular (LV) end-diastolic pressure (EDP) to those of stroke index (SI). In 4 normal cases the curves were steep, showing a fall of EDP with relatively large decrease of SI; in 3 cases of congestive myocardiopathy they were flat, showing fall of EDP in two and increase in one, with relatively small decrease of SI; in 5 patients with effort angina LVEDP initially decreased. This initial fall of VFCs was steep in two with normal and flattened in three with impaired resting LV function. Increase of EDP, evidently due to development of ischaemia, followed in all; it exceeded resting EDP in two out of three cases developing angina and in one out of two not developing angina. Our findings support the view that the increase of LVEDP is due to decrease of both myocardial contractility and compliance.
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PMID:Haemodynamic alterations of the left ventricle during right atrial pacing. 108 40

The function of both right and left sides of the heart was studied during spontaneous attacks of angina pectoris at rest in 7 patients showing ST depression (type I) and 4 showing ST elevation (type II) during the attack. In none of the 44 type I attacks and 29 type II attacks which were recorded did circulatory changes; the latter were different in the two groups. Type I attacks showed: a) a brief fall in arterial pressure, accompanied by b) a rise of right atrial and pulmonary wedge pressures and c) a decrease of cardiac output, right and left stroke work, the mean rate of systolic ejection, and indirect left ventricular pre-ejection dP/dt. In the course of the attack a hypertensive phase followed, which was paralleled by an increase of heart rate, cardiac output, left and right stroke work, and mean systolic ejection rate, left dP/dt; right atrial pressure and wedge pressure remained raised. All of the circulatory functions started to revert towards the pre-attack levels coincident with the waning phase of the electrocardiographic alteration, the latter occurring either spontaneously or after nitroglycerin. Type II attacks for the entire duration of the electrocardiographic changes showed: a) a reduction of arterial pressure, cardiac output, right and left stroke work, mean systolic ejection rate, and left dP/dt, b) a rise of right atrial and wedge pressures, and c) quite small changes of heart rate. When the electrocardiogram started to revert to the pre-attack aspect, the cardiac function rapidly improved and, after a supernormal phase, returned to the basal levels in about 2 minutes. It is concluded: 1) that no circulatory factor interfering with the mechanical effort of the heart is responsible for eliciting spontaneous angina: 2) that in type I attacks right and left ventricular impairment occurs which recovers rapidly, possibly through a sympathetic compensation; 3) that in type II attachs dysfunction of both sides of the heart occurs and persists throughout the episode of electrocardiographic alteration; 4) that the dynamic impairment is probably more severe in type I than in type II angina.
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PMID:Left and right heart haemodynamics during spontaneous angina pectoris. Comparison between angina with ST segment depression and angina with ST segment elevation. 112 17

Seven patients with coronary heart disease (CHD) but no angina pectoris had hemodynamic studies at rest and during submaximal and maximal exercise levels 2 mth after an acute uncomplicated myocardial infarction. The hemodynamic study was repeated after 3 mth of regular physical training. Maximal oxygen intake (VO2max) increased by 16.1% after physical training while maximal heart rate unsignificantly decreased (minus 3.3%). Higher VO2max after training resulted from an increase in maximal cardiac output (+7%) and stroke volume (+9.2%) and from a widening of the maximal arterio-venous oxygen (A-VO2) difference (+7.3%). The fall in stroke volume observed from submaximal to maximal exercise level was not affected by training. During submaximal exercise, the lower heart rate after training was attended by both a greater stroke volume and a wider A-VO2 difference; the cardiac output slightly decreased. We conclude that the increase in VO2max observed with early physical training in CHD results on one hand from an increased stroke volume whose specificity is not established, and on the other hand from a wider maximal A-VO2 difference; the latter is entirely due to a greater extraction of oxygen from the blood by the working muscles during maximal exercise.
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PMID:Early hemodynamic adaptations to physical training in patients with healed myocardial infarction. 114 68

To study the efficacy of isosorbide dinitrate in prevention of myocardial ischemia, 20 patients with angiographically proved coronary artery disease underwent atrial pacing (mean rate 138/min) before (P1), 10 minutes after (P2) and 65 minutes after (P3) sublingual administration of 5 mg of isosorbide dinitrate. The symptomatic, hemodynamic and metabolic responses were evaluated at rest and during each pacing period. Angina occurred in all subjects during P1. Angina did not recur or was less severe in 17 of 19 patients during P2 and in 19 of 20 patients during P3. Resting left ventricular end-diastolic pressure for the group was normal at 11 plus or minus 4 mm Hg (mean plus or minus standard deviation). On interruption of pacing at 4.5 minutes during P1, average end-diastolic pressure during sinus rhythm was abnormal (18 plus or minus 6 mm Hg). After administration of isosorbide dinitrate mean left ventricular end-diastolic pressure was significantly decreased at rest and remained normal when pacing was interrupted during P2 and P3. Brachial arterial pressure, cardiac index, tension-time index, left ventricular stroke work index and maximal rate of rise of left ventricular pressure were all diminished at rest before and during P2 and P3. S-T segment depression was less during P2 and P3 than during P1. Before isosorbide dinitrate was given, resting myocardial lactate extraction was 15 plus or minus 11 percent during P1 lactate extraction decreased to minus2 plus or minus 25 percent. Lactate extraction was significantly greater during P2 and P3 than during P1. This study demonstrates that sublingual administration of 5 mg of isosorbide dinitrate has a significant protective effect against pacing-induced myocardial ischemia at 10 and 65 minutes after administration.
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PMID:Effects of isosorbide dinitrate on the response to atrial pacing in coronary heart disease. 115 42


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