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Biomedical subjects

A Nitenberg

Publications and source records attributed to A Nitenberg.

At least 37 records · Page 2Linked to original sources
PubMed1997

Coronary vascular reserve is similarly reduced in hypertensive patients without any other coronary risk factors and in normotensive smokers and hypercholesterolemic patients with angiographically normal coronary arteries.

Hypertensive patients (HTP) with left ventricular hypertrophy have reduced coronary vascular reserve (CVR), but in HTP without left ventricular hypertrophy, CVR is within the normal range according to values determined in subjects without taking into account coronary risk factors such as cigarette smoking or hypercholesterolemia. To examine the influence of hypertension, cigarette smoking, and hypercholesterolemia on coronary flow and resistance reserve, coronary flow velocity was measured using a Doppler catheter before and after a maximally vasodilating dose of papaverine in 15 normotensive subjects without any coronary risk factors (Group 1), in 12 nonsmoker HTP with normal lipid profiles who had never been treated (Group 2), in 8 normotensive smoker patients (Group 3), in 9 normotensive nonsmoker patients with hypercholesterolemia (Group 4), and in 13 normotensive smoker patients with hypercholesterolemia (Group 5). All patients had normal coronary arteriography and left ventricular mass and function. Peak-to-resting coronary flow velocity ratio and mean aortic pressure were used to determine coronary flow reserve (CFR) and a minimal coronary vascular resistance index (MCVRI). Results show that in groups 2, 3, 4, and 5 comparatively to Group 1, CFR was similarly reduced (4.60 +/- 0.74 [P < .001], 4.59 +/- 0.35 [P < .001], 5.01 +/- 0.55 [P < .05], 5.03 +/- 0.78 [P < .05], groups 2 to 5, respectively, compared to group 1 5.66 +/- 0.68), and that MCVRI was similarly augmented (0.19 +/- 0.03 [P < .01], 0.20 +/- 0.0 [P < .001], 0.19 +/- 0.02 [P < .05], 0.19 +/- 0.03 [P < .05], groups 2 to 5, respectively, compared to group 1 0.16 +/- 0.02). In conclusion, HTP without left ventricular hypertrophy have a similar reduction of their CVR as smokers and hypercholesterolemic patients when compared to a group of subjects without any coronary risk factors. This should be taken into account when determining a group of control subjects for coronary reserve.

Adult↗
PubMed1997

[Ventriculoarterial coupling and left ventricular performance in hypertensive patients with left ventricular hypertrophy].

UNLABELLED: It has been shown that 1) contractile performance of hypertrophied left ventricle (LV) of hypertensive patients (HP) is depressed, and 2) ventriculoarterial (VA) coupling is altered when myocardial contractile performance is reduced and when afterload is increased. To assess the relationship between contractile performance of hypertrophied LV and the VA coupling in hypertensive patients. LV angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress/volume index ratio (ESS/ESVi), the slope of end-systolic pressure-volume relationship, i.e. end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Comparison of results in 30 HP and 20 control subjects (CS) showed that LV contractile performance assessed by Ees/100 g left ventricular myocardial mass (LVM, echocardiographic determination) was depressed (HT: 4.35 +/- 1.13; CS: 5.21 +/- 1.89 mmHg/ml/100 g; p < 0.02) and was negatively correlated to the LVM (Ees = -0.026 LVM + 3.363; r = 0.581; p < 0.001), when ESS/ESVi, another estimate of LV contractile performance, was comparable in the 2 groups (6.66 +/- 1.55 g/cm2/ml/m2 in HT vs 6.72 +/- 1.36 in CS; NS) and negatively correlated with the LVM (ESS/ESVi = -0.019 LVM + 8.947; r = 0.369; p < 0.01). Ventriculoarterial coupling evaluated through Ea/Ees ratio (Ea and Ees in mmHg/ml/m2) was slightly higher in HT (0.53 +/- 0.08 vs 0.48 +/- 0.09 in CS; p < 0.05), work efficiency (EW/PVA) was similar in the 2 groups (0.78 +/- 0.04 in HP vs 0.80 +/- 0.03 in CS) and PVA, which is representative of the myocardial oxygen demand per beat, is negatively related to LVM (PVA = -0.003 MVG + 1.44; r = 0.434; p < 0.01). CONCLUSIONS: this study shows that despite a slight depression of LV contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in HP with LV hypertrophy. Thus, it appears that LV hypertrophy might be a useful means of preservation of matching LV and arterial receptor with minimal energetical cost.

Blood Pressure↗
PubMed1997

[Response of the coronary arteries to cold test and flow velocity increase is improved by deferoxamine but not by L-arginine in diabetic patients].

UNLABELLED: Acetylcholine produces coronary artery (CA) constriction in diabetic patients suggesting an impairment of endothelium-dependent dilation. To examine the mechanism of this abnormal response. 2 physiological tests, i.e. cold pressor test (CPT) and coronary flow-increase induced by 10 mg papaverine (PAP) injection in the distal left anterior descending CA (dLAD), were performed before (1) and after (2) either i.v. L-arginine (L-arg, 625 mg/min x 10 min) or i.v. desferrioxamine (DFX, 50 mg/min x 10 min) in 15 normotensive nonsmoker diabetic patients with angiographically normal CA and normal cholesterol. Dimensions of the proximal LAD (pLAD) were measured by quantitative angiography. [table: see text] Before administration of L-arg or DFX, CPT induced a decrease of pLAD diameter, and PAP injection in dLAD dit not modify pLAD diameter. In the 7 diabetic patients receiving L-arg, responses to CPT and PAP were not modified. Conversely in the 10 patients receiving DFX, pLAD dilated in response to the 2 tests. Intracoronary isosorbide dinitrate, an endothelium-independent dilator, produced similar dilation in the 2 groups (+20 +/- 8% and +16 +/- 6%, respectively). CONCLUSIONS: 1) responses of angiography normal CA to CPT and to flow increase are impaired in diabetic patients; 2) abnormal responses are not improved by L-arg suggesting that a deficit in substrate for NO synthesis is not involved; 3) DFX restores a vasodilator response to the 2 tests suggesting that inactivation of NO by superoxide radicals might be partly responsible of the impairment of CA dilatation in diabetic patients.

Arginine↗
PubMed1997

Silent myocardial ischaemia and left ventricle hypertrophy in diabetic patients.

The purpose of this study was to evaluate the ability of three noninvasive techniques to detect silent myocardial ischaemia and analyse the factors associated with this condition, particularly left ventricular hypertrophy, in diabetic patients. An ECG stress test, a thallium-201 myocardial scintigraphy with dipyridamole intravenous infusion, ambulatory 48 h ECG monitoring and an echocardiographic study were performed in 92 diabetic patients without cardiac symptoms but with > or = 2 additional cardiovascular risk factors. At least one of these tests was positive in 28 patients (30.4%), suggesting silent myocardial ischaemia. Twenty-four of these patients had a coronary angiography which showed significant coronary stenosis in only 9 cases. An accurate echocardiographic tracing was obtained in 79 patients, particularly in 7 of the 9 with coronary stenosis. Left ventricular hypertrophy was detected in 34 patients, 6 of whom had coronary stenosis. In patients with left ventricular hypertrophy, the positive predictive values of myocardial scintigraphy and the ECG stress test were respectively 50% and 100%, as compared to only 33% and 11% in those without hypertrophy. In summary, coronary stenoses were found in < 10% of asymptomatic diabetic patients with > or = 2 cardiovascular risk factors, but more frequently in individuals with left ventricular hypertrophy. Thus, silent myocardial ischaemia should be searched for first in diabetic patients with hypertrophy, for which the stress test was the most accurate detection method in this study.

Adult↗
PubMed1997

[Coronary endothelial dysfunction in hypertension].

Intracoronary injection of acetylcholine leads to coronary vasodilatation in normal subjects and vasoconstriction in hypertensive subjects, suggesting an abnormality of endothelial function in hypertension. In order to study the response to physiological stimulation which induces endothelium-dependent vasodilatation, the effects of sympathetic stimulation (cold pressor test) and of the increase in flow velocity in the left anterior descending artery were analysed in 10 control and 26 hypertensive subjects. All had angiographically normal coronary arteries and normal lipid profiles. None of the subjects were smokers or diabetic. During the cold test (12 patients), the flow velocity increased by 47 +/- 26% (p < 0.05) in controls and by 68 +/- 48% (p < 0.01) in the hypertensives. Dilatation of the coronary arteries was observed in controls (+12.0 +/- 4.5%, p < 0.001) and constriction in the hypertensives (-10.3 +/- 8.5%, p < 0.001). Injection of papaverine in the distal left anterior descending artery (14 patients) induced proximal dilatation in controls (+17.0 +/- 10.6%, p < 0.001) and was ineffective in hypertensives (-0.4 +/- 1.5%), whereas the flow velocity increased by 521 +/- 129% and 406 +/- 120% (p < 0.001) respectively. Intracoronary injection of 2 mg of isosorbide dinitrate induced comparable dilatation in control subjects (+30.0 +/- 12.9%, p < 0.001) and in the 26 hypertensives (+22.8 +/- 6.5%, p < 0.001). In 10 hypertensive patients, intravenous injection of an angiotensin converting enzyme inhibitor, perindoprilat, immediately re-established the vasodilatory response to these two stimuli. The authors conclude that the coronary responses to physiological stimuli (sympathetic stimulation, increase in flow velocity) are altered in hypertensive subjects with angiographically normal coronary arteries with no other risk factors. Normal vasomotion may be restored by an angiotensin converting enzyme inhibitor.

Adult↗
PubMed1996

Angiotensin-converting enzyme inhibition restores flow-dependent and cold pressor test-induced dilations in coronary arteries of hypertensive patients.

BACKGROUND: Cold pressor test (CPT)-induced and flow-dependent epicardial coronary artery dilations are impaired in patients with hypertension. ACE inhibition can attenuate sympathetic coronary constriction and potentiate or restore endothelium-dependent relaxations. This study was designed to determine whether the ACE inhibitor perindoprilat can restore normal coronary dilative responses in hypertensive patients. METHODS AND RESULTS: Coronary vasomotor responses to CPT and to maximal increase of blood flow induced by papaverine were studied in 10 untreated patients with essential hypertension, no other risk factors, and angiographically normal coronary arteries before and after intravenous ACE inhibition by perindoprilat. Diameters of proximal and distal left anterior descending (LAD) and circumflex coronary arteries were measured by quantitative angiography. Estimates of coronary blood flow and resistance index were calculated with an intracoronary Doppler catheter in the distal LAD. Perindoprilat did not modify the hemodynamic responses to CPT and papaverine. In response to CPT, perindoprilat changed the epicardial coronary constriction (-8.4 +/- 5.8%, P < .001) into a significant dilation (+12.0 +/- 6.4%, P < .001). Perindoprilat significantly increased the coronary blood flow (from 33.7 +/- 10.0 to 57.9 +/- 20.5 mL/min, P < .01) and enhanced the decrease in coronary resistance (from 4.28 +/- 1.27 to 2.96 +/- 0.84 mm Hg.mL-1.min-1, P < .001) caused by CPT. Flow-dependent dilation of the proximal LAD was abolished in the control condition and was restored after perindoprilat (12.6 +/- 4.7%, P < .001). CONCLUSIONS: ACE inhibition restored CPT-induced and flow-mediated coronary artery dilations in patients with essential hypertension. These results indicate that impaired coronary vasomotor responses may be reversible in recently diagnosed hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Epicardial coronary arteries are not adequately sized in hypertensive patients.

OBJECTIVES: This study sought to compare coronary artery dimensions in hypertensive patients and normal subjects. BACKGROUND: Myocardial oxygen demand at rest and corresponding coronary blood flow are the main determinants of large coronary artery dimensions in humans. Coronary diameters are increased in aortic valve disease. METHODS: Left main, proximal and distal left anterior descending and proximal circumflex coronary artery diameters were measured by quantitative angiography in 10 control subjects (group 1) and 26 untreated hypertensive patients, 12 without (group 2a) and 14 with (group 2b) left ventricular hypertrophy. All patients had normal cholesterol levels and angiographically normal coronary arteries. Measurements were made at baseline and after 2 mg of intracoronary isosorbide dinitrate to obtain maximal dimensions of vessels. Coronary flow velocity was measured in the distal left anterior descending coronary artery by Doppler ultrasound. RESULTS: Despite a higher rate-pressure product in hypertensive patients, all segment diameters were slightly but not significantly higher at baseline in group 2b than in groups 1 and 2a. Diameters were similar in the three groups after isosorbide dinitrate. Conversely, coronary flow velocity was significantly higher in hypertensive patients than in group 1 either at baseline (10.4 +/- 2.2 [mean +/- SD] cm/s [group 2a] and 12.8 +/- 2.4 cm/s [group 2b] vs. 6.5 +/- 2.0 cm/s [group 1], all p < 0.001) or after isosorbide dinitrate (6.8 +/- 2.8 cm/s [group 2a] and 7.8 +/- 2.1 cm/s [group 2b] vs. 3.7 +/- 0.8 cm/s [group 1], p < 0.01 and p < 0.001, respectively). CONCLUSIONS: Despite an elevated myocardial oxygen demand, maximal dimensions of large coronary arteries are not increased in hypertensive patients, resulting in an elevated coronary flow velocity that may increase longitudinal shear stress at the endothelial surface. This elevated flow velocity might be an important determinant in the pathogenesis of atherosclerosis in hypertensive patients.

Blood Flow Velocity↗
PubMed1995

Loss of flow-dependent coronary artery dilatation in patients with hypertension.

BACKGROUND: Abnormal endothelium-dependent coronary response to acetylcholine has been shown in patients with essential hypertension. We tested the hypothesis that flow-dependent dilatation, which has been shown in normal human coronary arteries, is impaired in hypertensive patients. METHODS AND RESULTS: The coronary vasomotor response to maximal increase of blood flow induced by papaverine was studied in 10 control subjects and in 14 hypertensive patients with no other risk factors and angiographically normal coronary arteries. After the injection of papaverine in the midportion of the left anterior descending coronary artery (LAD), the diameter of the proximal LAD (LAD1) was measured by quantitative angiography, whereas that of the proximal circumflex artery (LCx) served as control segment. Estimates of coronary blood flow in the distal LAD (LAD2) were calculated by intracoronary Doppler flow velocity measurements. An increase in LAD2 blood flow of 521 +/- 41% (P < .001) in control subjects was associated with a 17.0 +/- 3.3% dilatation of the LAD1 (P < .001) and with no significant change in the diameter of the LCx. In hypertensive patients, despite a comparable increase in LAD2 blood flow of 406 +/- 32% (P < .001), the LAD1 failed to dilate (-0.4 +/- 0.6%, NS). The dilative response to isosorbide dinitrate was similar in control subjects and hypertensive patients (30.0 +/- 4.1%, P < .001 and 21.9 +/- 1.9%, P < .001, respectively). CONCLUSIONS: Thus, the flow-mediated coronary dilatation is lost in hypertensive patients, and this may impair normal dilatation observed in response to an increase in myocardial metabolic demand.

Adult↗
PubMed1995

Coronary artery response to cold-pressor test is impaired early after operation in heart transplant recipients.

OBJECTIVES: The aim of the present study was to evaluate the coronary vasomotor response to the cold-pressor test within 3 months after heart transplantation. BACKGROUND: Normal epicardial coronary arteries dilate in response to sympathetic stimulation evoked by the cold-pressor test. In transplant recipients, abnormal coronary vasomotion has been described shortly after operation. METHODS: Fourteen heart transplant recipients were compared 52 +/- 15 days (mean +/- SD) after operation with 10 control subjects. All had angiographically normal epicardial coronary arteries. Coronary blood flow velocity was measured with a Doppler catheter placed in the proximal left anterior descending coronary artery. Four segments in each patient were analyzed by quantitative coronary angiography to assess the diameter changes during the cold-pressor test and after intracoronary injection of isosorbide dinitrate. RESULTS: Coronary flow velocity increased similarly during the cold-pressor test in control subjects and in transplant recipients, from 7.5 +/- 2.3 to 11.0 +/- 3.9 cm/s and from 10.3 +/- 3.2 to 13.7 +/- 4.8 cm/s (both p < 0.01). In control subjects, 39 of 40 segments analyzed dilated during the cold-pressor test. In transplant recipients, 48 of 56 segments analyzed did not change or constricted. The mean epicardial coronary diameter increased significantly during the cold-pressor test in control subjects (+13 +/- 6%, p < 0.001), whereas it did not change significantly in transplant recipients (-2 +/- 9%, p = NS). In transplant recipients, isosorbide dinitrate elicited coronary vasodilation similar to that in control subjects. CONCLUSIONS: These data indicate that in human transplanted denervated hearts, coronary vasodilation in response to sympathetic stimulation by cold exposure is impaired shortly after operation.

Adult↗
PubMed1995

Impairment of flow-dependent coronary dilation in hypertensive patients. Demonstration by cold pressor test induced flow velocity increase.

In normal coronary arteries, increased flow velocity induces endothelium-dependent dilation, and dilation in response to sympathetic stimulation evoked by the cold pressor test is partly due to increased flow velocity. In arterial hypertension, angiographically normal coronary arteries were constricted by acetylcholine, an endothelium-dependent vasodilator. To assess the epicardial coronary artery response to the increase blood flow velocity induced by the cold pressor test in hypertensive patients with angiographically normal coronary arteries, coronary artery diameters and flow velocity were measured during cold pressor test in 12 untreated hypertensive patients and in 10 control subjects. Diameters were determined by quantitative angiography on proximal and distal segments of the left anterior descending coronary artery, and flow velocity measurements were made by Doppler testing in the distal segment. In control subjects, the proximal and distal segments dilated during cold pressor test by 12.0 +/- 4.5% and 13.9 +/- 6.5%, respectively (both P < .001), when flow velocity increased by 46.7 +/- 26.1% (P > .05). In hypertensive patients, segments were constricted, respectively, by 10.3 +/- 8.5% (P < .001) and 7.9 +/- 8.6% (P < .01), when the flow velocity was increased by 68.3 +/- 48.2% (P < .001). Intracoronary injection of an endothelium-independent dilator resulted in similar dilation in control subjects (proximal: +30.0 +/- 12.9%; distal: +32.4 +/- 15.2%) and in hypertensive patients (proximal: +22.3 +/- 7.5%; distal: +28.8 +/- 15.4%). In conclusion, in hypertensive patients with angiographically normal coronary arteries and without any other coronary risk factors, endothelium-dependent flow-mediated coronary dilation evoked by the cold pressor test is impaired.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1995

Coronary vascular reserve in humans: a critical review of methods of evaluation and of interpretation of the results.

The concept of coronary vascular reserve stems from the description of coronary autoregulation by Mosher in 1964. Schematically, the coronary blood flow at rest depends on the determinants of myocardial oxygen demand (heart rate, contractility and ventricular load). If maximal coronary vasodilation is produced, it results in a linear and steep pressure-flow relationship. The increment of coronary flow above its basal value is called the coronary flow reserve, which indicates the flow added to the basal flow for a given coronary perfusion pressure when the coronary vascular bed is maximally dilated. Thus, in the absence of epicardial coronary artery stenosis, the maximal coronary flow is a function of the coronary perfusion pressure and of the maximal surface area of the coronary circulation at the resistance vessel level. Evaluation of the coronary reserve in humans raises three major concerns: (1) methods for measuring or evaluating coronary flow are imprecise and inconvenient (diffusible indicators), invasive (coronary sinus thermodilution, intracoronary Doppler), expensive and require sophisticated technology (ultrafast computed tomography, positron emission tomography), or in the process of being validated (contrast echocardiography, transoesophageal Doppler echocardiography, myocardial scintigraphy: (2) the compounds used to produce maximal coronary vasodilation are administered either by the intracoronary route (papaverine) or intravenously (dipyridamole, adenosine); (3) how to interpret the data: is the alteration of the coronary reserve due to a modification of the basal coronary flow or/and of the maximal coronary flow? Thus, each method has its own limitations and constraints that must be taken into account in order to avoid crude misinterpretations. In conclusion, the measurement of coronary reserve may be an important means of understanding coronary physiology and pathophysiology. Recently developed non-invasive methods (ultrafast computed tomography, positron emission tomography, echography) and the ability to produce maximal coronary vasodilation by the intravenous route are promising.

Angiography, Digital Subtraction↗
PubMed1995

Dipyridamole slows the rate of isovolumic pressure fall in patients with normal coronary arteries.

Dipyridamole is currently used for thallium imaging and stress echocardiography. The coronary and haemodynamic effects of dipyridamole are well documented while its effects on left ventricular relaxation remain to be determined. The aim of the present study was to evaluate the effects of dipyridamole on left ventricular relaxation rate in healthy subjects. High fidelity pressure recordings were obtained at fixed atrial pacing (89 +/- 2 beats.min-1) in 10 subjects with normal left ventricular angiography and coronary arteriograms. Left ventricular pressure was recorded at rest and 5 min after a 4 min infusion of dipyridamole (0.14 mg.kg-1.min-1). Dipyridamole infusion decreased left ventricular systolic pressure (P < 0.01) and time to left ventricular systolic pressure (P < 0.01), with no changes in end-diastolic pressure or peak rate of pressure rise. The peak rate of isovolumic pressure fall decreased (from 1957 +/- 105 to 1488 +/- 100 mmHg.s-1, P < 0.01) and the time constant of isovolumic relaxation increased (from 37 +/- 2 to 44 +/- 3 ms, P < 0.02). In conclusion, our study indicates that acute administration of clinically relevant doses of dipyridamole displays deleterious effects on heart relaxation in healthy humans.

Arteries↗
PubMed1995

Early impairment of acetylcholine-induced endothelium-dependent coronary vasodilation is not predictive of secondary graft atherosclerosis.

STUDY OBJECTIVE: To test the hypothesis that the magnitude of early constriction of coronary arteries to acetylcholine might be a useful predictor of secondary graft atherosclerosis. DESIGN: The responses of epicardial coronary arteries to stepwise intracoronary infusion of acetylcholine (10(-8)M to 10(-5)M) were compared in 7 control subjects and in 18 patients who had undergone transplants within 2 months after surgery. MEASUREMENTS AND RESULTS: Vessel dimensions (percent basal diameter) were measured by quantitative angiography. Follow-up at 1 year showed angiographically normal coronary arteries in 12 patients (group 1) and coronary atherosclerosis in 6 patients (group 2). In control subjects, acetylcholine induced a dose-dependent dilation from 10(-8)M to 10(-6)M. No significant variation was observed at 10(-5)M. In patients with transplants early after surgery, diameters did not vary significantly from base at 10(-8)M in either group and constricted significantly at higher concentrations. Vasodilator responses to intracoronary isosorbide dinitrate were similar in both groups with transplants early after surgery, and at 1 year in group 1, but significantly lower than in control subjects. CONCLUSIONS: In patients who had undergone transplants, acetylcholine-induced endothelium-dependent coronary artery dilation is similarly impaired early after surgery (within 2 months) in patients with and without coronary atherosclerosis at 1-year follow-up. Thus, response to acetylcholine is not a predictor of secondary atherosclerosis in patients with heart transplants.

Acetylcholine↗
PubMed1995

[Restoration of normal coronary vasomotricity after intravenous infusion of angiotensin converting-enzyme inhibitor (perindoprilat) in hypertensive patients].

We have previously shown that in hypertensive patients, the response of normal coronary arteries to sympathetic stimulation evoked by the cold-pressor test (CPT), and the endothelial-mediated flow-dependent coronary vasodilation were impaired. The immediate effects of the converting-enzyme inhibitor perindoprilat (PER) have been evaluated in 10 untreated hypertensive patients with angiographically normal coronary arteries and results have been compared to the normal responses of 10 control subjects. Diameter changes of proximal left anterior descending coronary artery (pLAD) and coronary flow velocity in distal LAD have been measured at baseline, during CPT, during recontrol, and after 10 mg papaverine (PAP) injection in the mid portion of the LAD. Measures have been repeated after intravenous infusion of 1 mg PER, and at the end of the procedure after 2 mg intracoronary injection of isosorbide dinitrate (ISDN). Left ventricular dimensions and systolic function, total cholesterol, triglycerides, HDL and LDL-cholesterol were within the normal range. In hypertensive patients before PER, pLAD constricted in response to the CPT and no diameter change was observed after PAP, despite the increase in flow velocity in the 2 conditions (+63 +/- 27%, and +412 +/- 77%, respectively; all p < 0.001). In control subjects, pLAD dilated significantly in these 2 conditions. In hypertensive patients after PER, pLAD dilated similarly to control subjects in the 2 conditions. Endothelium-independent coronary dilation to ISDN was comparable in the 2 groups of patients. In conclusion, PER restores a normal coronary response both to sympathetic stimulation due to CPT and to flow increase in hypertensive patients with angiographically normal coronary arteries and without any other coronary risk factors.

Adult↗
PubMed1995

[Coronary artery caliber is not adapted to myocardial oxygen demand in hypertensive patients with angiographically normal coronary arteries].

Resting myocardial oxygen demand and corresponding coronary blood flow are main determinants of large coronary artery dimensions in humans. To examine the adaptation of epicardial coronary arteries to the increased myocardial oxygen demand, myocardial blood flow, in hypertensive patients, diameters of proximal and distal left anterior descending coronary artery (pLAD and dLAD), and proximal circumflex artery (CX) were determined in 15 untreated hypertensive patients and in 10 control subjects by quantitative angiography. All patients had total cholesterol < or = 5.40 mmol/l, LDL-cholesterol < or = 3.35 mmol/l, and angiographically normal coronary arteries. Measurements were made at base and after 2 mg intracoronary isosorbide dinitrate (ISDN) in order to obtain maximal dimensions of vessels. Coronary flow velocity was measured in distal left anterior descending coronary artery by Doppler. Results show that despite higher rate-pressure product in hypertensive patients, the diameters of the coronary segments were similar in control subjects and in hypertensive patients at base (3.53 +/- 0.84 vs 3.76 +/- 0.48 mm for pLAD; 2.55 +/- 0.50 vs 2.49 +/- 0.52 mm for dLAD; 2.92 +/- 0.40 vs 2.78 +/- 0.83 mm for CX, respectively). After intracoronary ISDN, diameters were also comparable between the 2 groups (4.54 +/- 0.86 vs 4.58 +/- 0.60 mm for pLAD; 3.35 +/- 0.58 vs 3.22 +/- 0.61 mm for dLAD; 3.47 +/- 0.56 vs 3.53 +/- 1.01 mm for CX, respectively). Conversely, coronary flow velocity was significantly higher in hypertensive patients at base (10.72 +/- 2.20 vs 6.48 +/- 2.01 cm/s; p < 0.001) and after ISDN (6.59 +/- 2.62 vs 3.72 +/- 0.87 cm/s; p < 0.001). Despite an elevated myocardial oxygen demand, large coronary artery dimensions are not increased in hypertensive patients resulting in an elevated coronary flow velocity that may increase longitudinal shear stress at the endothelial surface. This might be an important determinant in the pathogenesis of atherosclerosis in hypertensive patients.

Adaptation, Physiological↗
PubMed1994

Coronary artery constriction caused by the cold pressor test in human hypertension.

Hypertensive patients with angiographically normal coronary arteries may have myocardial ischemia when metabolic demand increases. Abnormal epicardial coronary artery vasomotion in response to sympathetic stimulation may contribute to ischemia in such patients. We studied the vasomotor response of smooth coronary arteries to a cold pressor test in 10 hypertensive patients without other risk factors and in 9 control subjects. Vessel dimensions were measured by quantitative angiography, and blood flow was calculated using an intracoronary Doppler catheter in the left anterior descending coronary artery. In response to cold pressor stimulation, arteries of control subjects dilated 13.0 +/- 5.9% (P < .001), and they constricted 8.2 +/- 8.5% in hypertensive patients (P < .001). Rate-pressure product increased from 9466 +/- 1677 to 12,547 +/- 2367 beats per minute (bpm).mm Hg in control subjects (P < .001) and from 13,720 +/- 1823 to 17,353 +/- 2037 bpm.mm Hg in hypertensive patients (P < .001). Coronary blood flow velocity and blood flow increased 51 +/- 26% (P < .05) and 87 +/- 27% (P < .001), respectively, in control subjects and 68 +/- 52% (P < .05) and 36 +/- 33% (P < .01) in hypertensive patients. At peak cold pressor test, despite a significant higher rate-pressure product in hypertensive patients, blood flow was similar in both groups, suggesting an uncoupling between myocardial metabolic demand and supply. Thus, hypertension impairs the vasodilator response of angiographically normal coronary arteries to a cold pressor test. This abnormal response may be due to enhanced catecholamine reactivity and/or impairment of endothelial flow-mediated vasodilator response.

Adult↗
PubMed1994

[Changes in coronary vasodilation in hypertensive patients with angiographically normal coronary arteries].

In normal subjects, coronary arteries dilate in response to sympathetic stimulation evoked by the cold pressor test. Similarly, in normal coronary arteries the increase in blood flow velocity induced by papaverine results in flow-dependent coronary dilation. In order to assess the coronary responses to both stimuli in hypertensive patients, variations of proximal left anterior descending coronary artery diameters and coronary blood flow velocity have been measured using quantitative coronary angiography and intracoronary Doppler in 10 control subjects and in 12 hypertensive patients. All the patients had angiographically normal coronary arteries. Total serum cholesterol, triglycerides, HDL- and LDL-cholesterol were within normal range in all patients. All patients were nonsmokers and none of them had diabetes mellitus. During the cold pressor test (hands immersed in ice water for 120 s), the rate-pressure product and coronary blood flow velocity increased respectively by 33 +/- 9% (p < 0.001) and 51 +/- 26% (p < 0.05) in control subjects, by 28 +/- 18% (p < 0.001) and 68 +/- 52% (p < 0.05) in hypertensive patients. In control subjects, coronary arteries dilated by + 12.0 +/- 4.4% (p < 0.001), and constricted by -10.3 +/- 8.5% (p < 0.001) in hypertensive patients. After injection of 10 mg of papaverine into the distal left anterior descending coronary artery, proximal left anterior descending coronary artery dilated by + 17.0 +/- 10.6% (p < 0.001) in control subjects, and did not vary (-0.7% +/- 10.6%) in hypertensive patients, when blood flow velocity was increased respectively by 449 +/- 97% and 383 +/- 103% (p < 0.001 in both groups).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗