PubMed Health⌕ Search

Biomedical subjects

A Nitenberg

Publications and source records attributed to A Nitenberg.

At least 73 records · Page 4Linked to original sources
PubMed1990

The use of midazolam and flumazenil in cardiovascular diagnostic and therapeutic procedures.

Sedation is sometimes required for cardiovascular diagnostic or therapeutic procedures. Midazolam may be proposed in these situations because of its duration of action and because of its moderate haemodynamic effects. However, the use of midazolam implies that the standards of safety required for all anaesthetic techniques have been applied. The changes in haemodynamic data induced by the administration of midazolam must be taken into account in interpretation of the catheterisation report. At the end of investigation, flumazenil can be administered safely to reverse residual sedative effects of midazolam but its use does not exempt from normal monitoring during the recovery period.

Cardiovascular Diseases↗
PubMed1990

Recovery of a normal coronary vascular reserve after rejection therapy in acute human cardiac allograft rejection.

During acute rejection, coronary vascular reserve is severely impaired in human orthotopic heart transplants. To evaluate the effects of rejection therapy on coronary vascular reserve, the ratio of peak-to-resting coronary flow velocity was assessed with a coronary Doppler catheter and a maximally vasodilating dose of intracoronary papaverine (12 mg) in nine allograft recipients without rejection (group 1) and in six recipients before and after treatment of an acute episode of rejection (group 2). All the patients had normal epicardial coronary arteries and were free of left ventricular hypertrophy. In group 2 during rejection, the coronary vascular reserve was significantly lower than in group 1, in which all the patients had a peak-to-resting coronary flow velocity ratio greater than 4 (2.3 +/- 0.5 vs. 5.4 +/- 0.8, respectively, p less than 0.001). In group 2 after treatment of rejection, the peak-to-resting coronary flow velocity ratio was similar to that of group 1 (4.7 +/- 0.8). Heart rate, left ventricular volumes and pressures, hemoglobin concentration, and arterial oxygen pressure were similar in the two groups. This study provides evidence that alterations of coronary vascular reserve because of acute rejection were reversible after treatment of the rejection episode.

Angiography↗
PubMed1989

Maximal coronary vasodilator capacity of orthotopic heart transplants in patients with and without rejection.

In cardiac allograft rejection, histopathologic changes suggesting that myocardial ischemia is a component of the rejection process have been documented. To further define the coronary vascular reactivity of human heart transplant, coronary sinus blood flow and coronary resistance were measured before and after intravenous dipyridamole within the first year after transplantation in 8 patients without rejection (group II) and in 5 patients with rejection (group III). All had normal coronary arteriograms. Results were compared to those of 8 control subjects (group I). After dipyridamole, coronary sinus blood flow was increased in groups I, II and III by 303, 212 (p less than 0.01 vs group I) and 45%, respectively (p less than 0.001 vs groups I and II). Coronary resistance was reduced by 77, 73 (not significant vs group I) and 36%, respectively (p less than 0.001 vs groups I and II). Concomitantly, coronary sinus blood oxygen content was increased by 172, 145 (not significant vs group I) and 78%, respectively (p less than 0.001 vs group I, not significant vs group II). Thus, the coronary flow reserve evaluated by the dipyridamole/basal coronary sinus blood flow ratio and the coronary resistance reserve evaluated by the basal/dipyridamole coronary resistance ratio were dramatically impaired in group III (1.56 +/- 0.09 and 1.63 +/- 0.30, respectively, p less than 0.001 vs groups I and II). In contrast, they were almost normal in group II (3.11 +/- 0.42 vs 4.03 +/- 0.52 in group I, p less than 0.02, and 3.83 +/- 0.78 vs 4.45 +/- 0.81 in group I, difference not significant). Thus, the impairment of coronary reserve during heart rejection should be linked to abnormalities of the coronary microvaculature. This emphasizes the important involvement of the coronary circulation in the rejection process.

Adult↗
PubMed1989

Selective infusion of tertatolol into the renal artery induces a local vasodilator effect in humans. Demonstration by the continuous thermodilution method.

The effects of tertatolol on renal circulation were studied in 8 patients with normal renal function. Left renal blood flow was measured by the continuous thermodilution method before (t0), and 5 (t1), 10 (t2) and 20 (t3) min after a selective infusion of 0.25 mg of tertatolol into the left renal artery. During the study, cardiac output, heart rate, aortic and right atrial pressures, systemic vascular resistances and the systemic arteriovenous oxygen difference were not significantly altered. Plasma renin activity and plasma aldosterone in arterial and renal venous blood started to decrease at t1. At t3, renal blood flow was increased (from 463 +/- 28 mL/min at t0, to 549 +/- 22 mL/min, P less than .001), renal vascular resistance was reduced (from 188 +/- 17 mm Hg/L/min at t0 to 156 +/- 15 mm Hg/L/min, P less than .01) and the arteriovenous oxygen difference was decreased (from 1.6 +/- 0.2 mL/100 mL at t0 to 1.1 +/- 0.1 100 mL, P less than .01). The renal/cardiac flow ratio increased from 10.0 +/- 2.2% to 11.7 +/- 2.1% (P less than .05) and the renal/systemic vascular resistance ratio decreased from 10.5 +/- 2.0 to 8.7 +/- 1.4 (P less than .01). These data show that selective infusion of a low dose of tertatolol into the renal artery results in an increase in renal blood flow which is delayed and occurs without concomitant changes in systemic hemodynamics. This suggests an intrarenal mechanism of action in humans supporting the previously observed renal vasodilation induced by tertatolol in isolated perfused animal kidneys.

Adult↗
PubMed1989

Coronary vasodilation induced by intracoronary enalaprilat: an argument for the role of a local renin-angiotensin system in patients with dilated cardiomyopathy.

Although indicated by several experimental studies, the presence of a renin-angiotensin system has not been demonstrated in the human heart. The influence of a local renin-angiotensin system on the coronary vessels may be difficult to establish after oral or intravenous administration of an angiotensin converting-enzyme inhibitor, since coronary blood flow depends greatly on the loading conditions of the left ventricle. To avoid such a situation, our study consisted in a direct bilateral intracoronary infusion of enalaprilat in patients with dilated cardiomyopathy and normal coronary arteries (mean ejection fraction = 32 +/- 11%, n = 12). This intracoronary infusion (0.05 mg min-1, 1 ml min-1 in each coronary artery) resulted in no significant change of the systemic resistances (20.6 +/- 5.6 to 22.0 +/- 5.1 mmHg l-1 min), rate-pressure product (10,974 +/- 2630 to 10,214 +/- 2486) or myocardial oxygen consumption (21.08 +/- 6.37 to 22.10 +/- 6.42 ml min-1). Despite these steady haemodynamic conditions, intracoronary enalaprilat provoked a significant elevation of coronary sinus blood flow (181 +/- 73 to 214 +/- 79 ml min-1, P less than 0.001) with a reduction of coronary resistance (0.51 +/- 0.17 to 0.41 +/- 0.15 mmHg ml-1 min, P less than 0.001), and no significant alteration in plasma renin activity or plasma aldosterone. The results of this intracoronary infusion of enalaprilat demonstrate that this angiotensin converting-enzyme inhibitor has significant coronary vasodilator properties, which can be evidenced without stimulating the peripheral renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomyopathy, Dilated↗
PubMed1989

Severe impairment of coronary reserve during rejection in patients with orthotopic heart transplant.

The present study analyzed coronary sinus blood flow alterations after dipyridamole induced coronary vasodilation in seven patients whose endomyocardial biopsies evidenced no sign of rejection (group 1) and in five patients with histologic signs of rejection (group 2) after orthotopic heart transplantation. All patients were treated with cyclosporine and prednisone and some with azathioprine and had normal coronary arteriograms. Coronary sinus blood flow and coronary resistance were measured before and after intravenous dipyridamole (0.18 mg/kg/min over 4 minutes). Basal values were similar in groups 1 and 2 for coronary sinus blood flow (166 +/- 34 compared with 181 +/- 39 ml/min, respectively), coronary resistance (0.62 +/- 10 compared with 0.52 +/- 13 mm Hg/ml/min, respectively), coronary sinus blood oxygen content (5.7 +/- 1.6 compared with 4.5 +/- 0.9 ml/100 ml, respectively) and arterial-coronary sinus blood oxygen difference (10.6 +/- 1.3 compared with 10.3 +/- 1.8 ml/100 ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1989

[Prognostic factors in dilated cardiomyopathy].

Thirty-eight patients, 27 men and 11 women, mean age 49 +/- 12 yr, suffering from dilated cardiomyopathy were included in this prospective study of prognostic factors. Twenty-two subjects admitted heavy alcohol consumption (greater than 80 g/d, for at least 10 yr). The survival rates for 2, 5 and 7 yr were 87, 35 and less than 20%, respectively. Prognostic factors were evaluated in 34 (22 alcoholic and 12 non-alcoholic) patients: 10 improved or were cured, as determined clinically, radiologically and echocardiographically (group 1); 24 deteriorated, 13 of whom died (group 2). Statistically significant values for group 1 versus group 2 were: echocardiographic left ventricular (LV) end diastolic diameter (3.50 +/- 0.80 vs 4.02 +/- 0.5 cm/m2, p less than 0.026) and LV end systolic diameter (2.97 +/- 0.65 vs 3.43 +/- 0.53 cm/m2, p less than 0.02); hemodynamic LV systolic pressure (113.9 +/- 15 vs 101.82 +/- 17.36 mm Hg, p = 0.045); angiographic LV end diastolic volume (137.8 +/- 57.44 vs 177.85 +/- 55.45 ml/m2, p = 0.057), LV end systolic volume 93 +/- 53.5 s 139.28 +/- 48.99 ml/m2, p less than or equal to 0.036), ejection fraction 0.36 +/- 0.16 vs 0.22 +/- 0.7%, p less than or equal to 0.006) and velocity of fiber shortening (0.79 +/- 0.53 vs 0.36 +/- 0.3 circ/s, p = 0.036). Other electrical, radiological and hemodynamic parameters were not significant and alcohol consumption did not influence the prognosis. The severity of LV functional impairment appears to be the major determinant of a poor prognosis and reduced survival in idiopathic and alcoholic cardiomyopathies.

Adult↗
PubMed1988

[Identification of prognostic criteria of dilated cardiomyopathies associated with chronic alcoholism. 22 cases].

Between November, 1978 and August, 1983, 22 patients aged from 28 to 65 years with idiopathic dilated cardiomyopathy diagnosed on the basis of clinical and haemodynamic criteria were investigated. All these patients, who consumed alcohol in excessive amounts, were followed up for 1 to 58 months. The overall mortality rate was 10 p. 100 at 4 months and 25 p. 100 at 58 months. Six patients were clinically improved with reduction of heart size (group A); 10 patients showed deterioration with 3 deaths (group C) and 6 patients followed an intermediate course (group B). When the characteristics of the groups were evaluated, it was found that compared to group C patients those in groups A and B had a lower cardiothoracic ratio: 0.56 +/- 0.04 (B) vs 0.64 +/- 0.06 (C) (P less than 0.02), a lower indexed end-diastolic diameter and systolic diameter on TM echo: 3.20 +/- 0.50 cm/m2 (A) vs 4.13 +/- 0.39 cm/m2 (C) (P less than 0.02), and 2.72 +/- 0.37 cm/m2 (A) vs 3.57 +/- 0.47 cm/m2 (C) (P less than 0.02) respectively, and a lower indexed end-diastolic volume as evaluated by angiography: 121 +/- 61 ml/m2 (A) vs 202 +/- 65 ml/m2 (C) (P less than 0.06). Dilated cardiomyopathy associated with excessive alcohol consumption has a better prognosis when the patients stop drinking and when their heart dilatation is mild to moderate.

Adult↗
PubMed1988

Doppler echocardiographic measurement of mitral flow volume: validation of a new method in adult patients.

Instantaneous intracardiac flow volumes can be calculated as the product of instantaneous flow velocity and instantaneous orifice area. This was accounted for in a new method of measuring stroke volume and cardiac output in the mitral orifice by pulsed Doppler echocardiography. This method was compared with simultaneous thermodilution in 30 adult patients in sinus rhythm without substantial atrioventricular or pulmonary valve abnormalities. The mitral orifice was assimilated to a conduit with 1) an ellipse-shaped inlet and outlet, 2) the same (and constant) long axis for the inlet and outlet ellipses (that is, the mediolateral anulus diameter measured on apical four chamber views), and 3) a varying outlet short axis (that is, the mitral anteroposterior leaflet separation derived from left parasternal M-mode recordings). This method design avoided the need for a short-axis view of the whole circumference of the mitral outlet orifice, which is difficult to obtain in many adult patients. The mitral flow velocity was recorded from the apex under two-dimensional guidance, within the mitral canal, close to the outlet section. Integration of instantaneous mitral leaflet separation multiplied by instantaneous flow velocity was performed using Simpson's rule. In addition to the proposed "instantaneous orifice area" method (method A), a "mean orifice area" method (method B) was also compared with thermodilution. In this simplified method, mitral flow was the product of mean orifice area and the diastolic mitral velocity integral, both derived from the same recordings as for method A.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Coronary flow and resistance reserve in patients with chronic aortic regurgitation, angina pectoris and normal coronary arteries.

Left ventricular hypertrophy has been found to be associated with a reduction of coronary vascular reserve, which could be responsible for episodes of myocardial ischemia. To evaluate coronary flow and resistance reserve in patients with chronic aortic regurgitation, coronary sinus blood flow and coronary resistance were measured before and after an intravenous dipyridamole infusion (0.14 mg/kg per min X 4 min) in eight control subjects and eight patients with aortic regurgitation, exertional angina pectoris and normal coronary arteriograms. Coronary flow reserve, evaluated by the dipyridamole/basal coronary sinus blood flow ratio, and coronary resistance reserve, evaluated by the basal/dipyridamole coronary resistance ratio, were both significantly reduced in patients with aortic regurgitation (1.67 +/- 0.40 versus 4.03 +/- 0.52 in control subjects, p less than 0.001 and 1.71 +/- 0.50 versus 4.38 +/- 0.88 in control subjects, p less than 0.001, respectively). In patients with aortic regurgitation, basal coronary sinus blood flow was higher than in control subjects (276 +/- 81 versus 105 +/- 24 ml/min, respectively, p less than 0.001) and basal coronary resistance was lower (0.31 +/- 0.13 versus 0.95 +/- 0.17 mm Hg/ml per min, respectively, p less than 0.001), but coronary blood flow and resistance after dipyridamole were not significantly different in the two groups (461 +/- 159 versus 418 +/- 98 ml/min in control subjects, 0.19 +/- 0.11 versus 0.22 +/- 0.04 mm Hg/ml per min in control subjects, respectively). These data demonstrate that coronary reserve is severely reduced in patients with chronic aortic regurgitation and exertional angina.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Reversibility by dipyridamole of thallium-201 myocardial scan defects in patients with sarcoidosis.

PURPOSE: In order to clarify the significance of anginal pain and myocardial thallium-201 scan defects in cardiac sarcoidosis, the pharmacologic effect of dipyridamole on myocardial perfusion was assessed by planar thallium-201 myocardial scintigraphy in patients with sarcoidosis. PATIENTS AND METHODS: Thallium-201 myocardial scintigraphy was performed at rest and after 0.56 mg/kg intravenous dipyridamole during four minutes in 16 patients with sarcoidosis. The myocardial scan (45-degree and 70-degree left anterior oblique, and anterior views) was divided into 15 segments. Results were evaluated by the number of segmental defects and with a global perfusion score (from 0 to 60) by a semi-quantitative index depending on the size and severity of myocardial thallium-201 defects. RESULTS: Thirteen of the 16 patients showed partial or total reversion of their thallium-201 defects on redistribution scanning either at rest or after dipyridamole. The mean (+/- SD) number of myocardial perfusion defects that were present in all the patients decreased from 5.31 +/- 1.78 at rest to 3.25 +/- 2.52 after redistribution (p less than 0.001) and to 2.19 +/- 2.10 after dipyridamole (p less than 0.001). The mean global perfusion score increased from 53.2 +/- 3.0 at rest to 56.2 +/- 2.9 after redistribution (p less than 0.001) and to 57.2 +/- 2.7 after dipyridamole (p less than 0.001). A significant correlation (r = 0.82, p less than 0.001) was found between the increase of global perfusion score on redistribution and after dipyridamole. CONCLUSION: The reversibility of myocardial scan defects is a common finding in sarcoidosis. It makes unlikely the role of scar fibrosis or extensive confluent granulomas as a mechanism for such defects. The effect of dipyridamole suggests the presence of reversible disorders lying at the coronary microvascular level.

Adult↗
PubMed1988

Direct myocardial and coronary effects of enalaprilat in patients with dilated cardiomyopathy: assessment by a bilateral intracoronary infusion technique.

Angiotensin II elicits contractile responses in the coronary arteries and myocardial tissue, which suggests that blockade of the renin-angiotensin system by specific agents should lead to both coronary vasodilation and an alteration of left ventricular inotropism. The present work was designed to delineate--independently from its systemic effects--the intrinsic actions of an angiotensin converting-enzyme inhibitor on the coronary circulation and left ventricular function. To minimize peripheral effects, a bilateral intracoronary infusion of enalaprilat (0.05 mg.min-1, 1 ml.min-1 in each coronary artery) was performed in 16 patients with dilated cardiomyopathy. All patients had normal coronary arteriograms. In 12 patients (group I) the intracoronary infusion of enalaprilat resulted in minimal peripheral changes, with a 5% reduction in the mean aortic pressure (p less than .05) and no significant alteration in indexes of preload, i.e., left ventricular end-diastolic pressure and volume, or of afterload, i.e., left ventricular end-systolic stress and systemic resistances. Myocardial oxygen consumption was also unaffected by the intracoronary infusion of enalaprilat. Coronary vasodilation was demonstrated by a significant elevation of coronary sinus blood flow (+19%, from 181 +/- 73 to 214 +/- 79 ml.min-1, p less than .001) and a reduction of coronary resistance (-18%, from 0.51 +/- 0.17 to 0.41 +/- 0.15 mm Hg.ml-1.min, p less than .001), with a parallel increase in coronary sinus oxygen content and pressure (both p less than .05). Oxygen extraction by the myocardium was reduced (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Myocardial microvascularization in scleroderma].

Myocardial involvement in systemic sclerosis may be caused, at least in part, by myocardial ischemia due to functional or structural abnormalities of small coronary arteries or arterioles. Coronary reserve, assessed by dipyridamole-induced coronary vasodilatation, was strikingly impaired in patients with systemic sclerosis. Thallium scans have shown numerous myocardial perfusion defects in scleroderma patients. Two studies, using oral nifedipine and intravenous dipyridamole, demonstrated that these thallium-201 myocardial perfusion defects in patients with systemic sclerosis were partially reversible. Finally, the preliminary results of long-term studies suggest that some coronary vasodilators may be beneficial in the long-term treatment of myocardial perfusion abnormalities in systemic sclerosis.

Coronary Circulation↗
PubMed1987

[Coronary reserve: a dynamic evaluation of coronary circulation].

Measuring the coronary reserve is a way of evaluating pathologies of the large coronary vessels as well as of coronary microcirculation. In man, measurement of the coronary sinus blood flow by the thermodilution method can be used to determine the increase in flow induced by selective injection of a contrast medium into the left coronary artery or by intravenous injection of dipyridamole. Such measurements have been performed in subjects with normal coronary blood flow and left ventricular function, in patients with cardiac or systemic diseases likely to alter coronary perfusion (e.g. atheromatous coronary disease, dilated cardiomyopathy, scleroderma, sarcoidosis) and in patients who had undergone heart transplantation. Flow and resistance reserves have been calculated from the maximal/basal coronary flows ratio and from the minimal/basal coronary resistance ratio. The results obtained provided information on the repercussions of coronary stenosis on myocardial perfusion and on alterations of coronary microcirculation in pathologies respecting the main coronary arteries. In addition, changes in coronary reserve induced by some pharmacological agents may be used to evaluate the effects of certain cardiovascular therapies.

Cardiomyopathy, Dilated↗
PubMed1987

[Non-obstructive hypertrophic cardiomyopathy and systolic compression of 3 coronary arteries. Long-term improvement with verapamil].

Systolic compression of the three main coronary vessels was observed during the investigation of a 23 year old African with hypertrophic cardiomyopathy. The patient was admitted in 1982 for evaluation of retrosternal chest pain and one syncopal attack during exercise. The ECG showed left ventricular hypertrophy with important ST-T wave changes which became more severe on exercise. Diffuse myocardial hypertrophy without obstruction was confirmed by echocardiography and cardiac catheterisation. Coronary angiography showed systolic compression of the three main coronary arteries. There was no coronary vasodilatory response to rapid atrial pacing; increased left ventricular end diastolic pressure confirmed the poor tolerance of exercise. The therapeutic failure of betablockers suggested a possible coronary spasm. Long-term (4 years) clinical improvement was obtained with calcium antagonists (Verapamil 360 mg/day) without significant regression of the hypertrophy. Coronary vasodilation under Verapamil led to improved tolerance of rapid atrial pacing. Control angiography showed only mild systolic compression of the three main coronary vessels. The improvement of this functional coronary insufficiency with Verapamil was attributed to its negative inotropic effects associated with improved myocardial relaxation and ventricular filling.

Adult↗