Search PubMed⌕ Search

Biomedical subjects

A Nitenberg

Publications and source records attributed to A Nitenberg.

At least 91 records · Page 5Linked to original sources

[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↗

Nifedipine and thallium-201 myocardial perfusion in progressive systemic sclerosis.

Heart disease in patients with progressive systemic sclerosis may be due in part to myocardial ischemia caused by a disturbance of the coronary microcirculation. To determine whether abnormalities of myocardial perfusion in this disorder are potentially reversible, we evaluated the effect of the coronary vasodilator nifedipine on myocardial perfusion assessed by thallium-201 scanning in 20 patients. Thallium-201 single-photon-emission computerized tomography was performed under control conditions and 90 minutes after 20 mg of oral nifedipine. The mean (+/- SD) number of left ventricular segments with perfusion defects decreased from 5.3 +/- 2.0 to 3.3 +/- 2.2 after nifedipine (P = 0.0003). Perfusion abnormalities were quantified by a perfusion score (0 to 2.0) assigned to each left ventricular segment and by a global perfusion score (0 to 18) for the entire left ventricle. The mean perfusion score in segments with resting defects increased from 0.97 +/- 0.24 to 1.26 +/- 0.44 after nifedipine (P less than 0.00001). The mean global perfusion score increased from 11.2 +/- 1.7 to 12.8 +/- 2.4 after nifedipine (P = 0.003). The global perfusion score increased by at least 2.0 in 10 patients and decreased by at least 2.0 in only 1. These observations reveal short-term improvement in thallium-201 myocardial perfusion with nifedipine in patients with progressive systemic sclerosis. The results are consistent with a potentially reversible abnormality of coronary vasomotion in this disorder, but the long-term therapeutic effects of nifedipine remain to be determined.

Adult↗

Dipyridamole versus intracoronary injection of contrast medium for the evaluation of coronary reserve in man: a comparative study.

Coronary reserve can be assessed by the ratio of coronary blood flow after "maximum" vasodilation to control flow. The intravenous infusion of dipyridamole (0.56 mg X kg-1) is considered to elicit maximum coronary vasodilation. The present study was designed to compare coronary flow and resistance responses to intravenous dipyridamole and intracoronary injection of contrast medium (ioxaglate), this latter technique being frequently used in digital radiology to stimulate hyperemia. The comparison was performed in seven normal patients, nine patients with coronary artery disease, and 16 patients with dilated cardiomyopathy. Coronary flow reserve was calculated as the ratio of peak flow after dipyridamole or contrast medium to control flow, and coronary resistance reserve was calculated as the ratio of minimal to control coronary resistance after each stimulus. Although flow reserve after dipyridamole was approximately twice that obtained after contrast medium in the normal group (4.01 +/- 0.56 vs 2.02 +/- 0.24) there was a close and linear relationship between coronary flow and resistance reserve estimated by both techniques (r = 0.846, p less than 0.001 for flow reserve ratios, and r = 0.844 p less than 0.001 for resistance reserve ratios). However, contrast-induced hyperemia identified 13/25 (52%) of patients with coronary artery disease or dilated cardiomyopathy as having a reduced flow reserve, while dipyridamole revealed a restrained coronary flow reserve in 20/25 (80%) of these patients. Similar proportions were obtained when using coronary resistance reserve (56% for contrast vs 80% for dipyridamole). (ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Reduced coronary flow and resistance reserve in primary scleroderma myocardial disease.

The maximum coronary vasodilator capacity after intravenous dipyridamole (0.14 mg X kg-1 X min-1 X 4 minutes) was studied in seven patients with primary scleroderma myocardial disease and compared to that of seven control subjects. Hemodynamic data and left ventricular angiographic data were not different in the two groups. The coronary flow reserve was evaluated by the dipyridamole/basal coronary sinus blood flow ratio (D/B CSBF) and the coronary resistance reserve by the dipyridamole/basal coronary resistance ratio (D/B CR). Coronary reserve was greatly impaired in the group with primary scleroderma myocardial disease: D/B CSBF was lower than in the control group (2.54 +/- 1.37 vs 4.01 +/- 0.56, respectively; p less than 0.05) and D/B CR was higher than in the control group (0.47 +/- 0.25 vs 0.23 +/- 0.04, respectively; p less than 0.05). Such a decreased coronary flow and resistance reserve in patients with primary scleroderma myocardial disease was not explained by an alteration of left ventricular function. It may be an important contributing factor in the pathogenesis of primary scleroderma myocardial disease.

Adult↗

Effect of diltiazem on coronary reactive hyperemia in patients with flow-limiting coronary artery stenosis.

The acute effects of diltiazem on coronary reactive hyperemia were studied in 12 patients with flow-limiting coronary stenosis. Reactive hyperemia was elicited by injection of 8 ml contrast medium into the left coronary artery, while coronary sinus blood flow and left ventricular and aortic pressures were continuously recorded. Relative magnitude of hyperemia was estimated by the ratio of coronary flow at peak hyperemia to baseline flow (hyperemic ratio). Coronary resistance was calculated as the ratio between mean aortic pressure minus left ventricular mean diastolic pressure and coronary sinus blood flow. The 12 patients studied had flow-limiting coronary stenosis since their hyperemic ratio was significantly restrained when compared to that of seven control subjects (1.45 +/- 0.17 vs 2.02 +/- 0.24, respectively; p less than 0.001). The intravenous infusion of diltiazem (0.30 mg X kg-1) reduced heart rate, mean aortic pressure, and myocardial oxygen consumption (all p less than 0.001). After diltiazem the hyperemic ratio was blunted when compared to the basal state (1.36 +/- 0.15 vs 1.45 +/- 0.17, respectively; p less than 0.05), and hyperemia volume was reduced (-33%; p less than 0.001). The decrease in coronary resistance at peak hyperemia was also reduced from -30 +/- 8% to -25 +/- 8% (p less than 0.05). We conclude that diltiazem blunts coronary reactive hyperemia in patients with demonstrated flow-limiting coronary stenosis. This reduction of coronary flow response to a hyperemic stimulus could favorably influence blood flow distribution in patients with significant coronary stenosis.

Adult↗

Effects of midazolam on the coronary circulation in patients with coronary artery disease.

The effects of midazolam on coronary sinus blood flow (CSBF), myocardial oxygen consumption (MVO2), and myocardial lactate balance were investigated in eight patients with stable coronary artery disease undergoing cardiac catheterization. Coronary sinus blood flow was measured by continuous thermodilution. Arterial and coronary sinus blood were analyzed for oxygen and lactate content. The determinants of left ventricular (LV) performance were obtained from the cardiac output measured by thermodilution and from left heart catheterization data. All data were obtained before, and 5 and 15 min after midazolam, 0.2 mg X kg-1 iv. Sleep was induced in all patients after administration of midazolam and persisted throughout the entire study period. Mean aortic and LV end-diastolic pressure were decreased from control values (-15 and -44%, respectively), as well as cardiac index and stroke index (-10 and -15%, respectively). Heart rate increased moderately (+8%), while no change in systemic vascular resistance and maximum velocity of shortening (Vmax) were observed. Midazolam administration was followed by a decrease of CSBF (-24%) and of MVO2 (-26%). Coronary vascular resistance did not change, but coronary sinus oxygen tension increased slightly, suggesting a mild alteration in normal autoregulation. However, no evidence of myocardial ischemia occurred, as judged by the absence of changes in the: 1) ECG, 2) myocardial lactate extraction, and 3) relaxation time constant. These results suggest that midazolam may be used safely in patients with coronary artery disease.

Anesthesia↗

Dipyridamole-induced coronary vasodilation in human transplanted heart: preliminary report.

Coronary sinus blood flow and resistance were studied before and after intravenous dipyridamole in 4 patients with transplanted heart and normal coronary arteriogram treated by cyclosporine-prednisolone. Results were compared to those of a normal group of 7 subjects. Left ventricular endomyocardial biopsies were performed in the heart transplanted group. Mean right atrial pressure, cardiac index and left ventricular function were normal in the transplanted heart group. Mean aortic pressure and systemic vascular resistances were significantly higher in the transplanted group than in normals (p less than 0.01), but coronary resistance were similar. Dipyridamole-induced vasodilation resulted in an increased coronary sinus blood flow and a decreased coronary resistance in both groups, but these effects were reduced in 1 patient with a transplanted heart that evidenced an important perivascular fibrosis after a subacute rejection. In conclusion, this preliminary report of coronary blood flow in patients with transplanted heart indicates that the ability of coronary sinus blood flow to increase after dipyridamole is normal in the transplanted heart without allograft rejection. A major limitation in coronary vasodilation was observed in 1 patient with rejection antecedents and perivascular fibrosis, which could play a role in left ventricular function deterioration in some patients after heart transplantation.

Adult↗

[The coronary hyperemic reaction in scleroderma].

Functional, organic and vascular anomalies could play an important role in systemic scleroderma. We have studied the coronary hyperemic reaction in subjects with primitive sclerodermatous cardiomyopathy, in order to specify the vascular anomalies. The coronary hyperemic reaction consists of a transient rise in coronary flow after selective injection of a contrast agent into the left coronary artery. In sclerodermatous subjects this coronary hyperemic reaction is significantly smaller than in control subjects. This limitation of the hyperemic reaction reflects a decrease in the ability of small arteries or coronary arterioles to dilate in sclerodermatous subjects. This anomaly could play an important role in primitive sclerodermatous cardiomyopathy.

Cardiac Catheterization↗

Multifactorial determinants of reduced coronary flow reserve after dipyridamole in dilated cardiomyopathy.

Coronary sinus blood flow (ml/100 g left ventricular [LV] mass/min) and coronary resistance (mean aortic minus LV mean diastolic pressures/coronary sinus blood flow, mm Hg/[ml/100 g/min]) were studied in 7 control patients and in 11 patients with severe dilated cardiomyopathy (DC) and normal coronary arteriograms. Basal coronary sinus blood flow was not different in the 2 groups. After intravenous administration of dipyridamole (0.14 mg/kg/min X 4 min), coronary sinus blood flow and dipyridamole/basal coronary sinus blood flow ratio were significantly (p less than 0.001) lower in the DC group than in the normal group (coronary sinus blood flow 188 +/- 48 vs 408 +/- 58, respectively; blood flow ratio 1.78 +/- 0.35 vs 4.01 +/- 0.56, respectively), and the coronary resistance was higher in the DC group than in the control group (0.39 +/- 0.15 vs 0.22 +/- 0.03, respectively, p less than 0.01). After administration of dipyridamole in patients with DC, no correlation could be found between coronary sinus blood flow and LV mean diastolic, mean aortic or coronary driving pressures, i.e., mean aortic minus LV mean diastolic pressures. Thus, in DC patients, neither an elevated LV diastolic pressure nor a low coronary perfusion pressure can totally account for the restriction of the coronary flow reserve after dipyridamole.

Adult↗

Decreased coronary reserve in primary scleroderma myocardial disease.

We assessed coronary reserve, by measuring the increase in coronary sinus blood flow (CSBF) after intravenous administration of dipyridamole (0.14 mg/kg/minute for 4 minutes), in 7 patients with primary scleroderma myocardial disease (PSMD) and in 7 control subjects. Coronary reserve was greatly impaired in PSMD: before administration of dipyridamole, CSBF was similar in patients with PSMD (89 +/- 32 ml/minute/100 gm, mean +/- SD) and in controls (100 +/- 15 ml/minute/100 gm); after dipyridamole infusion, CSBF was significantly lower in patients with PSMD (191 +/- 45 ml/minute/100 gm) than in controls (399 +/- 58 ml/minute/100 gm) (P less than 0.01). Six of the 7 patients with PSMD had angiographically normal epicardial coronary arteries and normal left ventricular function. Decreased coronary reserve may be an important contributor to the pathogenesis of primary scleroderma myocardial disease.

Adult↗

Cardiac sarcoidosis: reversion of myocardial perfusion abnormalities by dipyridamole.

A Tl 201 scan was performed on one young patient who met all of the criteria for the diagnosis sarcoidosis. A resting scan before treatment showed marked defects which were not resolved on the redistribution scan, thus leading to the diagnosis of cardiac sarcoidosis, which was also suspected from clinical signs. After dipyridamole infusion (0.142 mg/kg per minute over 4 min), his 201Tl scan was quite normal. Haemodynamic investigation showed a low coronary sinus blood flow with a low lactate extraction: these abnormalities were fully reversed by i.v. dipyridamole infusion. Afterwards, the patient was given oral dipyridamole (450 mg/day) over 4 weeks; at the end of this treatment, his resting 201Tl scan was quite normal. These results suggest that myocardial perfusion abnormalities in sarcoidosis may be reversible after pharmacological vasodilation. Thus, in order to assess cardiac sarcoidosis, a resting myocardial scan should be performed before a scan after dipyridamole infusion. These results may have clinical, pathophysiological and therapeutic implications with regard to cardiac sarcoidosis.

Adult↗

Alterations in contrast medium-induced coronary reactive hyperemia after bepridil in patients with coronary artery disease.

The acute effects of an intravenous infusion of bepridil (BEP) (4 mg . kg-1) on left ventricular (LV) hemodynamics, coronary sinus blood flow (CSBF), and myocardial metabolism were studied in eight patients with coronary artery disease. In contrast with data previously reported with calcium channel blockers, BEP induced an elevation in LV end-diastolic pressure from 12.0 +/- 7.1 to 20.1 +/- 7.2 mm Hg (mean +/- SD, p less than 0.001) and a fall in LV dp/dt max from 1339 +/- 302 to 1177 +/- 251 mm Hg . sec-1 (p less than 0.01). This significant alteration in LV function is likely to be explained by the lack of effect on heart rate and aortic pressure observed after an acute intravenous infusion of BEP. Myocardial oxygen consumption (MVO2) increased from 448 +/- 272 to 498 +/- 273 mumol . min-1/100 g LV (p less than 0.05) as did CSBF from 79.5 +/- 42.7 to 92.1 +/- 45.1 ml X min-1/100 g LV (p less than 0.01). Lactate extraction fell from 0.33 +/- 0.17 to 0.15 +/- 0.17 (p less than 0.05). A contrast medium-induced coronary reactive hyperemia (HPR) evidenced an increased hyperemic volume from 9.5 +/- 3.6 to 12.1 +/- 4.5 ml/100 g LV (p less than 0.01) and HPR duration from 23.3 +/- 6.9 to 32.3 +/- 15.4 sec (p less than 0.05) after BEP. However, the peak/resting CSBF ratio was blunted after BEP from 1.74 +/- 0.18 to 1.61 +/- 0.12 (p less than 0.05), evidencing a net effect of BEP on HPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Assessment and follow-up of patients with aortic regurgitation by an updated Doppler echocardiographic measurement of the regurgitant fraction in the aortic arch.

The purpose of this study was to determine the value and limitations of an updated Doppler echocardiographic measurement of the aortic regurgitant fraction derived from the comparison of forward and reverse flows in the aortic arch. The method was based on the improvements in sampling and displaying Doppler frequencies and blood velocities provided by pulsed-emission, two-dimensional location, and spectral analysis and on an account for variations of aortic diameter through an M mode record of the aortic arch. Relevant statistical comparisons were performed between simultaneous noninvasive and invasive determinations of the regurgitant fraction in a group of 30 patients with aortic regurgitation (group I) and between simultaneous noninvasive and invasive measurements of variations of the regurgitant fraction induced by atrial pacing or vasodilator administration in 12 patients of this group. The two basal determinations were closely correlated (r = .90). The invasive regurgitant fraction ranged from 0% to 80%. The standard error of the Doppler estimate was 8.8% in group I as a whole and was only 6% in a subgroup of 20 patients with a high systolic aortic flow pattern, defined as both peak velocity above 0.8 m/sec and duration of systolic flow above 0.24 sec. This pattern was present in almost all (19/22) patients in whom the aortic regurgitation was more than moderate by invasive criterion (regurgitant fraction above 40%). The standard error of the Doppler estimate of variations of the regurgitant fraction was only 6.6%. Among 100 additional patients with aortic regurgitation (group II), only 12 had no pandiastolic reverse flow in the arch, and their regurgitation was always mild at aortographic examination.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Non-invasive measurement of cardiac output by Doppler echography].

In this review paper the theoretical and technical bases of cardiac output measurement in the thoracic extracted from the literature and obtained by the authors themselves are summarized. The main physiological assumptions required for calculations (flat velocity profile in the aorta) and the main technical options (pulsed or continuous emission of ultrasounds, spectral or simplified Doppler signal analysis, evaluation or non-evaluation of the angle of incidence by two-dimensional imaging, echographic mode of measurement of the aortic diameter) are discussed. The need for controlled studies of each equipment and method on large populations of patients is emphasized.

Adult↗

Analysis of increased myocardial contractility during sodium acetate infusion in humans.

To analyze the reported effects of acetate on left ventricular (LV) contractility during dialysis, LV function was studied before and after a 20-min sodium acetate (Na Ac) infusion (0.06 mmoles X kg-1 X min-1) in seven patients with heart rate (HR) controlled by atrial pacing. Angiographically determined LV volumes and LV pressures were used to calculate the LV function indices. A plasma acetate concentration of 3.13 +/- 1.05 (SD) mmoles X liter-1 induced an increase in cardiac index from 3.8 +/- 0.6 to 4.4 +/- 0.6 (SD) liter X min-1 X m-2 (P less than 0.01) and a rise in total body O2 consumption from 7.47 +/- 1.28 to 8.67 +/- 1.66 mmoles X min-1 X m-2 (P less than 0.05); there was no alteration of the volume elastic constant, of the end diastolic stress, and of the end systolic stress. There was an increase of the ejection fraction from 0.44 +/- 0.10 to 0.51 +/- 0.09 (P less than 0.01), the maximum velocity of shortening (Vmax, sec-1) from 1.37 +/- 0.25 to 1.55 +/- 0.28 (P less than 0.05), and of the end systolic stress-end systolic volume ratio (g X cm-2 X ml-1) from 2.99 +/- 0.76 to 3.40 +/- 0.98 (P less than 0.01). Hence, the enhancement of these indices was not the consequence of any alteration of HR, preload, or afterload.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗