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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 15 patients with acute myocardial infarction associated with signs of left ventricular dysfunction, phentolamine was infused intravenously in a dose of 10 mg per hour. This therapy induced a substantial reduction in mean right atrial pressure from 10 to 7 mmHg (1.3 to 0.9 kPa) (P) less than 0.001), and in pulmonary capillary wedge pressure from 20 to 13 mmHg (2.7 to 1.7 kPa) (P less than 0.001). The cardiac index increased from 2.5 to 3.0 1/min per m-minus 2 (P less than 0.001) accompanied by a fall in both the systemic and pulmonary vascular resistances (P less than 0.001). On the other hand, the mean stroke work index did not change significantly after phentolamine, because of tar resistance. With the dose used the mean arterial pressure decreased from 112 to 99 mmHg (14.9 to 13.2 kPa) (P less than 0.001). No adverse effects attributable to the drug treatment were noted. Benefits of this treatment are probably related to reduction in the impedance of left ventricular ejection and possibly to its relaxant effect on the venous tone. The drug may also improve subendocardial perfusion by decreasing left diastolic ventricular pressure. This could possibly limit extension of necrosis. Thus vasodilator therapy appears to be of particular interest in left ventricular failure complicating acute myocardial infarction, where inotropic agents may be contraindicated.
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PMID:Phentolamine for vasodilator therapy in left ventricular failure complicating acute myocardial infarction. Haemodynamic study. 114 63

The effects of the positive-inotropic drug Canrenoat-Kalium (CRK) on the extent and severity of myocardial ischemic injury and on hemodynamic parameters were studied in 17 dogs following coronary occlusion. Acute myocardial infarction causes depression of left-ventricular function. There eas a significant decrease in dp/dtmax, stroke volume and cardiac output; average values for mean arterial pressure were reduced, but not significantly. There was a significant increase in left-ventricular enddiastolic pressure. Heart rate was unchanged. In the healing phase of myocardial infarction a significant elevation of left-ventricular enddiastolic pressure and a significant decrease of arterial pressure persisted, but the other parameters had returned toward normal. Intravenous administration of CRK (20 mg/kg) one hour after coronary occlusion causes a significant increase in left-ventricular dp/dtmax, cardiac output and stroke volume, but no significant change in arterial pressure, heart rate and left-ventricular enddiastolic pressure. Four days after myocardial infarction administration of CRK causes also a significant incrrease in left-ventricular dp/dtmax and -n 4 out of 5 animals an increase in stroke volume. Heart rate, arterial pressure and left-ventricular enddiastolic pressure are unchanged. There is a continuous deterioration of all hemodynamic parameters in the control group 1 hour and 96 hours after experimental myocardial infarction. This spontaneous deterioration has to be taken into consideration estimating the effect of CRK in experimental conditions. 120 epicardial electrocardiographic recordings were used to assess the extent and severity of myocardial ischemic injury. The average ST-segment elevation and the number of sites with abnormal ST-segments were significantly reduced 20 min after CRK administration. The study suggests a beneficial therapeutic role for CRK treatment of left-ventricular failure in the acute and healing phase after myocardial infarction.
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PMID:[Influence of canrenoate potassium (aldactone pro injections) on hemodynamics and myocardial ischemia in experimental myocardial infarct]. 116 92

Haemodynamic changes after intravenous administration of 0.4 mg beta-methyldigoxin or 0.4 mg digoxin daily were measured on the first to fourth day in 42 patients in heart failure after onset of transmural myocardial infarction. Regular reduction in filling pressure and increased stroke volume while arterial blood pressure remained unaltered pointed to improved contractility. Digitalization in the first few days after infarction achieved sustained tendency towards improved haemodynamics. It is concluded that early digitalization is indicated in patients with acute myocardial infarction if there are signs of heart failure.
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PMID:[Digitalization for acute myocardial infarction: haemodynamic changes in patients with heart failure at rest (author's transl)]. 118 55

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significane of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean +/- SD): (SEE ARTICLE). Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index less than or equal to 2.0 liters/min/m2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m2 (p less than 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p less than 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The "booster pump" function of the atrium cannot be ignored in assessing left ventricular performance.
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PMID:Left atrial transport function in myocardial infarction. Importance of its booster pump function. 120 36

Left ventricular performance in 16 patients with uncomplicated acute myocardial infarction (AMI) has been estimated, by measuring the haemodynamic response to a moderate increase in left ventricular filling pressure (LVFP), obtained by an espansion in blood volume with a slow infusion of 250 ml of plasma. In 9 cases the infusion was repeated. This represents a total of 25 tests. In 17 tests (group A) cardiac index (CI) and left ventricular stroke work index (LVSWI) did not increase significantly and sometimes decreased. In 8 tests (group B) The same plasma volume expansion (PVE) induced a moderate but significant increase in CI(p less than 0.001) and LVSWI (p less than 0.001). A higher incidence of inferior wall infarction was present in group B. Control CI and LVFP did not differ between the two groups and there was no correlation between the initial LVFP and the type of response to PVE. For the same volume load, the increase in pulmonary capillary wedge pressure (CWP) showed large individual variations (+1 to +8 mm Hg). As a general rule when CI improved, the increment in CWP was minimal (+1 mm Hg). It is concluded that there is no unique optimal LVFP and that PVE must be carefully monitored, in all cases.
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PMID:Haemodynamic response to slow plasma volume expansion in uncomplicated myocardial infarction. 120 60

In 70 patients hemodynamic controls were preformed during the first 4 days after acute myocardial infarction. A sufficient regulation of heart function and the circulation at rest was accepted with the following conditions: pulmonary artery wedge pressure less than or equal to 13mm Hg, mean right atrial pressure less than or equal to 6 mm Hg, mean systemic arterial pressure greater than 70 mm Hg, cardiac index greater than 2.51/min/m2 and stroke index greater than 25 ml/m2. In 88% of the patients with acute myocardial infarction a cardiac failure was present at rest. The pressures in the right atrium and left atrium (from wedge pressures) were elevated and cardiac output was reduced. The ratio of stroke work index/mean pulmonary artery wedge pressure allowed a more precise differentiation between a compensated and failing heart (X +/- S = 3.6 +/- 0.7 resp. 1.7 +/- 0.6 g m/m2 mm Hg). In the average, a significant improvement of the hemodynamic alterations, due or not due to therapy, occurred only at the 3rd day or later. In the individual case, this improvement points to a favorable prognosis.
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PMID:[Hemodynamic evaluation of cardiac insufficiency in the acute stage of myocardial infarct]. 122 62

Selective coronarography, left ventricular cineangiography were performed three to six months after acute myocardial infarction in 45 patients. Simultaneously, stroke volume (SV), enddiastolic (EDV) and endsystolic volume (ESV), ejection fraction (EF) and left ventricular enddiastolic pressure (LVEDP) were determined. LVEDP was measured at rest and after static (handgrip) exercise. According to the type of the LV abnormality patients were divided in three groups: 1. without LV abnormality (5 patients) 2. asynergy (15 pts) and 3. aneurysm (25 pts). The data were reviewed separately in patients where abnormalities of LV were associated with angina pectoris. The degree of coronary obstruction and the type of LV abnormality did not disclose any correlation. LVEDP at rest was in normal limits in patients in group 1 and 2, elevated in patients with aneurysm. (LVEDP: 15, 15 and 25 mmHg resp.) After handgrip exercise LVEDP increased in each group: 21, 22, 32 mm Hg. SV: decreased significantly in LV aneurysm (53 ml/beat). EDV was 50 ml in patients with asynergy and 118 ml in those with aneurysm. ESV was in normal limits when asynergy was present, 35 ml in patients without abnormality and 118 ml in LV aneurysm. EF was 0.66 and 0.65 in group 1 and 2, in group 3 (aneurysm) this value was 0.49 (significantly lower). The extent of shortening of the longitudinal and transverse diameters were significantly diminished in each group. When angina was associated with LV asynergy a higher SV was observed, when angina was associated with aneurysm, SV and EF were decreased. The conclusion from these data can be drown that the compromised LV after prior AMI works with a different mechanism, according the type (and degree) of abnormality.
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PMID:Abnormalities of left ventricular function associated with prior acute myocardial infarction. 123 42

In 20 patients with acute myocardial infarction requiring emergency left heart catheterization and coronary arteriography, ventricular function and clinical course were related to collateral vessels supplying the infarcted area. The major coronary artery to the infarcted region was severely obstructed in all patients. Patients with adequate collateral vessels (Group I, no. = 6) and those with no or inadequate collateral channels (Group II, no. = 14) had similar findings with respect to age, site of infarction, prevalence of prior infarction and presence of multivessel disease. However, there were significant differences between Groups I and II in left ventricular end-diastolic pressure (13 versus 30 mm Hg), cardiac index (3.05 versus 2.04 liters/min per m2), stroke work index (45 versus 13 g-m/m2), ejection fraction (42 versus 20 percent) and area of dyssynergy (14 versus 47 percent). Moreover, in Group I all patients survived and none had cardiogenic shock, whereas in Group II 10 of 14 patients had shock and 8 of 14 died. The rapidity of vessel obstruction appeared to influence collateralization since infarction was preceded by angina pectoris more frequently in Group I than in Group II. These results indicate that well functioning anastomotic channels to the distal trunk of the blocked coronary artery may afford some protection of pump function and improve the prognosis in acute myocardial infarction.
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PMID:Functional significance of coronary collateral vessels in patients with acute myocardial infarction: relation to pump performance, cardiogenic shock and survival. 125 68

Forty-three patients with severe pump failure complicating acute myocardial infarction were treated with vasodilators (nitroprusside (40) and phentolamine (3)) for four hours to 27 days. Cardiac index, stroke volume index, and stroke work index (SWI) increased while the left ventricular filling pressure (LVFP) decreased during vasodilator therapy. Twenty-four of the 43 patients (56%) survived. Of patients with initial SWI between 11-20 gm-m/m2 and LVFP less than 15 mm Hg, 68% survived. In contrast only 18% of patients with SWI of 10 gm-m/m2 or less and LVFP greater than 15 mm Hg survived. Of the 17 patients with clinical shock, 8 (47%) survived. All 24 patients discharged from the hospital were followed for at least 12 months. Fourteen patients died one to 25 months (average 9.2 months) after discharge and the cause of death was pump failure in ten of them (71%). The ten survivors at last follow-up had been followed for 15 to 32 months (average 24 months). The cumulative survival at 24 months was 28%. Thus, despite improvement in short-term prognosis with vasodilator therapy in patients with severe pump failure complicating acute myocardial infarction, the prognosis for long term survival remains unfavorable, possibly due to severe intrinsic cardiac damage.
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PMID:Effects of vasodilator therapy for severe pump failure in acute myocardial infarction on short-term and late prognosis. 126 Sep 83

Intra-aortic balloon counterpulsation (IABP) was used in 20 patients with acute myocardial infarction and cardiogenic shock, after four hours of drug treatment. In all instances the abnormal haemodynamic state had been demonstrated. Four patients were successfully treated and finally discharged home. In two with post-infarction ventricular septal defect and cardiogenic shock, IABP also successfully reversed the shock state, while in seven the shock state was reversed but they died 2-8 days after IABP had been stopped. IABP failed in seven patients who died during its application. In those in whom IABP failed there had been no significant fall in pulmonary-artery pressure and no significant increase in stroke volume. The post-mortem examinations demonstrated that cardiogenic shock was irreversible where more than 50% of the left ventricular myocardium had been infarcted.
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PMID:[Treatment of cardiogenic shock after acute myocardial infarction with intra-aortic balloon counterpulsation (author's transl)]. 126 28


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