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Biomedical subjects

A Nitenberg

Publications and source records attributed to A Nitenberg.

At least 55 records · Page 3Linked to original sources
PubMed1991

[Coronary reserve in treated hypertension with persistent left ventricular hypertrophy].

UNLABELLED: It has been demonstrated that coronary reserve (CR) is impaired in hypertensive patients with left ventricular hypertrophy and normal epicardial coronary arteries. The present study was undertaken in order to determine if CR returns to normal level after antihypertensive therapy in patients with persistent left ventricular hypertrophy, when the decrease of arterial blood pressure induces a reduction of LV wall stress (LVWS). In 26 patients with normal coronary arteriography, end-diastolic wall thickness (EDWT), LV mass (LVM) and peak systolic LVWS were determined on 30 degrees right anterior oblique LV angiography with simultaneous recording of LV pressure (micromanometer). Coronary flow velocity was measured with a coronary doppler catheter before and after a maximally vasodilating dose of intracoronary papaverine (12 mg). The study group included 6 untreated (G1) and 7 treated (G2) hypertensive patients with LV hypertrophy, and 13 control subjects (C). The peak-to-resting coronary flow velocity ratio (P/R) and a minimal coronary vascular resistance index (MCVRI) calculated as the quotient of mean aortic pressure at peak flow velocity to peak flow velocity and mean aortic pressure at resting flow velocity to resting flow velocity were assessed. Results evidenced that in hypertensive patients with LV hypertrophy, levels of P/R and MCVRI were similar in treated and untreated groups. Thus, in treated patients P/R remained lower and MCVRI remained higher than in control subjects despite the normalization of arterial pressure that resulted in a low peak systolic LVWS. [table: see text] CONCLUSION: this study demonstrates that anti-hypertensive therapy does not restore a normal coronary vascular reserve in patients with persistent LV hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1991

[Coronary disease in patient following heart transplantation].

Coronary artery disease is a common and particularly severe complication of cardiac transplantation because it may cause progressive destruction of the graft by acute or chronic ischemia. The ischemia is usually silent because of cardiac denervation. Cardiac failure related to graft dysfunction, asymptomatic infarction on the ECG, or sudden death, are sometimes the only signs of severe coronary disease. The prevalence of coronary lesions has been evaluated by coronary angiography at nearly 25% at 2 years and 50% at 5 years. The distribution and morphology of the lesions are characteristic: diffuse concentric, irregular and occlusive, predominantly distal stenoses, without a distal and usually without a collateral circulation. The histological features are variable: the association of medial necrosis, severe endothelial lesions and intense parietal inflammation are suggestive of acute arteriolitis, often present during acute rejection, may be related to a common pathological process. Diffuse obliterative arteriolar lesions with concentric proliferation of medial smooth muscle are the usual appearances in transplant patients who have died or been retransplanted. There is no non-invasive diagnostic method sufficiently sensitive of specific which justifies the practice of many groups of systematic annual coronary angiography in transplanted patients. The pathogenesis is poorly understood and probably multifactorial: disorders of lipid metabolism, immunological factors, the atherogenic role of Cytomegalovirus infection. The absence of an identifiable risk factor makes preventive measures difficult. The evolutive risk justifies retransplantation in selected patients, the results of which are less satisfactory but which reduces the risk of acute coronary events and sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗
PubMed1991

[The functional renal reserve].

The term "renal functional reserve" (RFR) refers commonly to the reserve of glomerular filtration rate (GFR) and renal blood flow. RFR can be elicited by an oral protein load or by infusion of amino acids, glucagon, or dopamine. The increase in GFR which follows amino acid administration results from a cascade of events including pancreatic release of glucagon, involvement of an hepatic step, and renal synthesis of vasodilatory prostaglandins. RFR represents a constant fraction of baseline GFR as long as the latter is above 40-50 ml/min. RFR becomes virtual for lower values of GFR. It has been suggested that permanent challenge of RFR, which occurs in protein-rich diet or during the hyperfiltration phase of diabetic nephropathy, might lead to and accelerate impairment of renal function. The relevance of RFR measurement as a tool to predict the evolution of renal function in various types of renal diseases remains to be evaluated.

Amino Acids↗
PubMed1990

Effect of plasma volume expansion on hemodynamics and atrial natriuretic factor release in heart-transplant recipients.

Plasma atrial natriuretic factor (ANF), plasma cyclic guanosine monophosphate (cGMP), plasma aldosterone, plasma-renin activity (PRA) and hemodynamic parameters were measured in heart-transplant recipients and control patients (chest pain syndrome) during right-sided heart catheterization under basal conditions and in response to an intravenous saline load. Basal plasma ANF and cGMP were higher in heart-transplant recipients than in control patients, whereas PRA and plasma aldosterone did not differ. The high plasma ANF levels in heart-transplant recipients did not result from high atrial pressures but appeared to be related with elevated atrial dimensions and cyclosporine-induced renal failure. During volume expansion, plasma ANF increased in control patients and remained elevated during the postinfusion period. In heart-transplant recipients, the changes in plasma ANF were less marked despite identical increases of atrial pressures. The sluggish response of plasma ANF in this group was associated in the postinfusion period with a nonreturn of the hemodynamic parameters to their basal values in contrast with what was observed in control patients.

Adult↗
PubMed1990

Beta blockers induce different intrarenal effects in humans: demonstration by selective infusion of tertatolol and propranolol.

The effects of tertatolol and propranolol on renal circulation were studied in patients with normal renal function to test the hypothesis that various beta blockers may have different vasomotor effects within the renal vascular bed. Left renal blood flow was measured by the continuous thermodilution method before (t0), and 5 (t1), 10 (t2), 20 (t3), and 30 (t4) minutes after a selective infusion of tertatolol (0.25 mg, N = 4) or propranolol (2.5 mg, N = 4) into the left renal artery. Heart rate, cardiac output, aortic and right atrial pressures, and systemic vascular resistances did not significantly vary after either drug throughout the study. Plasma renin activity and plasma aldosterone in arterial and renal venous blood started to decrease at t1 after each drug. After propranolol, renal blood flow, renal vascular resistance and the renal arteriovenous oxygen difference were unchanged. Conversely, after tertatolol at t3, renal blood flow was increased (from 426 +/- 18 mL/min/1.73 m2 to 509 +/- 56 mL/min/1.73 m2, P = .03), renal vascular resistance and renal arteriovenous oxygen difference were decreased (P less than .001), and the renal blood flow/cardiac output ratio was increased (P = .03). The filtration fraction did not vary after either drug, as attested by the unchanged polyfructosan extraction coefficient. This clinical study shows that selective infusion of a single low dose of tertatolol into the renal artery results in a delayed intrarenal vasodilator effect, while at the dose tested propranolol does not modify renal hemodynamics.

Adrenergic beta-Antagonists↗
PubMed1990

Size dependence of the end-systolic stress/volume ratio in humans: implications for the evaluation of myocardial contractile performance in pressure and volume overload.

The end-systolic stress/volume ratio is currently recognized as a relatively load-independent index of myocardial contractile performance, but its dependence on ventricular size may limit its value for interpatient comparisons. In this study, the relation between the end-systolic stress/volume ratio and left ventricular end-diastolic volume was angiographically analyzed in 104 patients with normal coronary angiograms. Eighteen patients had a normal ventricle, 24 had aortic stenosis, 18 had aortic regurgitation, 9 had mitral regurgitation and 35 had cardiomyopathy. An inverse relation between the end-systolic stress/volume ratio and left ventricular end-diastolic volume was demonstrated in the normal group (r = 0.72, p less than 0.001); subjects with a larger left ventricle had a reduced index but, presumably, the same degree of contractility as that of subjects with a smaller ventricle. Attempts to normalize values by using end-diastolic volume or body surface area were unsuccessful. A similar inverse relation was demonstrated in the aortic stenosis group (r = 0.48, p less than 0.05), probably because hypertrophy helps to keep wall stress normal or low despite progressive ventricular enlargement in these patients. The end-systolic stress/volume ratio was also inversely related to left ventricular chamber size in patients with volume overload due to aortic regurgitation (r = 0.80, p less than 0.001) and in those with cardiomyopathy (r = 0.84, p less than 0.001). However, at a given left ventricular end-diastolic volume, the end-systolic stress/volume ratio was higher in patients with aortic regurgitation than in those with cardiomyopathy, suggesting better contractile performance for a comparable degree of ventricular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Glucagon secretion is essential for aminoacid-induced hyperfiltration in man.

The role of glucagon as a mediator of aminoacid-induced alteration of renal haemodynamics was evaluated in man in three different protocols. In the first it was shown that the increase in glomerular filtration rate (GFR) and renal plasma flow (RPF) observed during an aminoacid infusion was prevented by the additional infusion of somatostatin (SRIF), but reproduced by a glucagon infusion in the presence of SRIF. In the second protocol it was shown that, at variance with normal subjects, six totally pancreatectomised patients, thus deprived of pancreatic glucagon secretion, did not increase their GFR and RPF when infused with amino-acids, whereas they exhibited the expected hyperfiltration when infused with glucagon. In the third protocol it was shown that glucagon infusion in a renal artery did not alter the homolateral renal haemodynamics. It is concluded that glucagon secretion is a mandatory step in the cascade of events linking the infusion of aminoacids to the renal hyperfiltration. Other steps beyond glucagon secretion are necessarily involved because glucagon has no direct renal effect.

Adult↗
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↗