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Biomedical subjects

I Antony

Publications and source records attributed to I Antony.

At least 19 recordsLinked to original sources
PubMed2001

Left ventricular mechanical efficiency in hypertensive patients with and without increased myocardial mass and with normal pump function.

Left ventricular hypertrophy (LVH) is a physiologic process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular contractile performance, mechanical efficiency and ventriculoarterial coupling are preserved in hypertensive patients with LVH. To assess the differences between patients with and without LVH, left ventricular contractile performance and the ventriculoarterial coupling were compared in two groups of hypertensive patients with similar body surface area and arterial pressures, and normal pump function: 30 patients with LVH (group 1) and 23 without LVH (group 2). Left ventricular angiography coupled with simultaneous recording of pressures with a micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW), and pressure-volume area (PVA). Myocardial contractile performance, assessed by Ees normalized by myocardial mass and by ESSVR, was lower in group I than in group 2 (1.23 +/- 0.28 v 1.89 +/- 0.48 mm Hg/mL/100 g, and 3.85 +/- 0.99 v 5.13 +/- 0.56 g/cm2/mL, respectively, both P < .001). Ventriculoarterial coupling evaluated through Ea/Ees ratio, and mechanical efficiency evaluated through EW/PVA ratio, were similar in the two groups (0.53 +/- 0.08 v 0.51 +/- 0.05, and 0.78 +/- 0.03 v 0.80 +/- 0.02, respectively, NS). In conclusion, this study shows that ventriculoarterial coupling and mechanical efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in hypertensive patients, the matching between left ventricular performance and arterial load and the energy transfer are preserved either through left ventricular hypertrophy with moderate depression of myocardial contractile performance or through enhancement of myocardial contractile performance in patients with normal left ventricular mass.

Adult↗
PubMed2001

Impairment of coronary microvascular dilation in response to cold pressor--induced sympathetic stimulation in type 2 diabetic patients with abnormal stress thallium imaging.

Coronary microcirculation dysfunction may be associated with myocardial perfusion defects on thallium imaging in diabetic patients without coronary artery stenosis. Microvascular coronary adaptation to increased myocardial oxygen demand in response to sympathetic stimulation evoked by the cold pressor test was examined in 22 type 2 diabetic patients with thallium imaging defects and in 15 control subjects. Both the diabetic patients and control subjects had angiographically normal coronary arteries and no other risk factors. Despite a similar increase in the rate-pressure product in the two groups (22.6 +/- 12.4% in diabetic patients and 31.8 +/- 8.2% in control subjects, NS), coronary blood flow increase in the left anterior descending artery (mean flow velocity measured by intracoronary Doppler multiplied by the cross-sectional area measured by digital angiography) was significantly lower in diabetic patients than in control subjects (14.7 +/- 19.8 vs. 75.5 +/- 13.5%, respectively; P = 0.0001). In addition, when there was a positive correlation between the two parameters in control subjects (r = 0.651, P < 0.01), there was no relationship in diabetic patients (r = 0.054). In conclusion, vasodilation of the coronary microcirculation in response to sympathetic stimulation evoked by the cold pressor test is impaired in type 2 diabetic patients without epicardial artery lesions. This microvascular impairment during sympathetic stimulation may explain exercise-induced myocardial perfusion abnormalities observed in these patients and may impair microcirculatory coronary vasodilation during current life stress episodes such as exercise, mental stress, or cold exposition.

Blood Flow Velocity↗
PubMed2001

[Inhibition of iron-catalyzed oxidative reactions restores mathcing between coronary blood flow and myocardial metabolic demand in type 2 diabetes].

In diabetes, endothelium-dependent dilation of large and small coronary arteries is impaired, which results in a mismatch between myocardial metabolic demand and coronary blood flow. It has been proved that deferoxamine, an iron chelator that inhibits Fenton and Haber-Weiss reactions, restores a normal response to cold pressor test and flow increase in angiographically normal epicardial coronary arteries of diabetic patients. This result suggests that nitric oxide could be inactivated by reactive oxygen species. The aim of this study was to assess the effects of deferoxamine on coronary microcirculation vasomotion when myocardial oxygen demand is increased by sympathetic stimulation elicited by cold pressor test in type 2 diabetic patients. In 17 patients with angiographically normal coronary arteries and without any other coronary risk factors, coronary blood flow has been measured using quantitative angiography and intracoronary Doppler at baseline and during a cold pressor test, before and after intravenous administration of 500 mg deferoxamine. Increase in rate-pressure product, an estimate of myocardial metabolic demand, was similar before and after deferoxamine (+21.1 +/- 8.7% vs +20.5 +/- 8.9%, respectively), but coronary blood flow increase was significantly higher after deferoxamine (+6.3 +/- 12.9% vs +31.8 +/- 16.7%, respectively, p < 0.001), and coronary resistance was increased before deferoxamine and decreased after (+14.8 +/- 21.9% vs -7.9 +/- 10.9%, respectively, p < 0.001). Moreover, before deferoxamine, the negative correlation between coronary blood flow and rate-pressure product changes before deferoxamine (R = 0.518, P < 0.05) was turned in a positive relationship after deferoxamine (r = 0.546, p < 0.05). In conclusion, in type 2 diabetic patients, endothelium-dependent dilation of the coronary microcirculation is restored when iron-catalysed oxidative reactions are inhibited by deferoxamine, which restores the normal matching between myocardial oxygen demand and coronary blood flow.

Adult↗
PubMed2001

[The REVEIL study: feasibility study of blood pressure self-monitoring. Preliminary results and patient opinions].

The REVEIL study is a pilot studies to determine the feasibility of self blood pressure measurement (SBPM). Feasibility was assessed by the quality of measurements and the patient opinion. This preliminary report focused on the patient opinion. Patients were included in the study by their general practitioner or cardiologist when he thought there was an indication for SBPM. Patients were excluded if their physical or mental autonomy was not sufficient to perform SBPM or if they were arrhythmic. The lending of the device was free (against a guarantee of 800 F) and it was available in one of the 44 drugstores that participated to the study. The physician performed patient education about SBPM and the druggist explained the handling of the device. SBPM was performed over a 7-day period: every day two series of 3 consecutive measurements were requested in the morning before taking the antihypertensive treatment, and in the evening between dinner and bedtime. The device was the validated OMRON 705 CP. 428 patients were included in the study. Among them, 385 (90%) accepted to participate to the study and 43 refused (10%). Almost half of the refusals were due to patients that did not want to take care of them and 16% were justified by a technical problem. Preliminary data included 362 patients aged 55.2 years, 79 of them older than 70 years. 80 patients (22%) experienced difficulties to perform SBPM, 28 of them (7.3%) to perform measurements and 13 (3.4%) to understand how worked the device. At the end of the study, 82 patients (23%) had better understanding of their hypertension, 90 patients (25%) felt themselves more motivated to take their medication and 111 patients (31%) found that their physician took better charge of them. 286 patients (79%) evaluated the overall satisfaction at SBPM. Among them, 276 patients (97%) were very satisfied (57%) or satisfied (40%) with SBPM when only 3% of patients were not. In summary, SBPM was easily performed in the conditions of the REVEIL study, and the majority of patients was satisfied with this experience.

Antihypertensive Agents↗
PubMed2001

[REVEIL Trial: Study validity, information and logistics. Preliminary results. Quality measures].

Self blood pressure measurement (SBPM) is not fully applied because of the cost of devices and the lack of efficient dedicated medical networks. The aim of the REVEIL study was to allow patients to freely rent SBPM devices by their pharmacist after initial medical prescription. Practitioners taught SBPM methods to the patients with a booklet and the pharmacist explained them how to use the device. This preliminary report focuses on the 428 first patients included from September 1999 to June 2000 by their general practitioner (n = 59) or cardiologist (n = 12) in the centre of the city of Reims (France), when he thought there was an indication for a SBPM period. The patient received a medical prescription and took a validated device (Omron 705CP) by one of the 44 pharmacists who accepted to participate. After 7 days the patient consulted his practitioner with the filled booklet. The prescription was for 7 days with 3 measurements each morning (before intake of antihypertensive drugs) and each evening (12 hours later). Patients reported the results on the booklet and enclosed the report printed by the device. From the 428 included patients, 362 (85%) gave analyzable data, the difference being explained by refusals (n = 39) and by the lag between inclusion and completion. Mean age was 55.2 (range 20 to 90). Education levels were: no graduation (n = 71), primary school (n = 172), college (n = 59), university (n = 86) [no answer in n = 40]. Seventy nine percent (n = 286) performed at least 12 measurements on three consecutive days. There is no significant difference between morning and evening completions. According to themselves, 294 patients fully succeeded in SBPM. Eighteen failed (6 reported a failure of the device, 2 had not understood the procedure, 5 had forgotten, 5 reported another cause), 50 did not answer. These results establish the fair applicability of SBPM under the realistic conditions of the REVEIL study (free rent of devices after medical prescription) as 85% of patients gave contributive information with a good quality in 79% of them.

Adult↗
PubMed2000

Restoration of flow-dependent coronary dilation by ACE inhibition improves papaverine-induced maximal coronary blood flow in hypertensive patients: demonstration that large epicardial coronary arteries are more than conductance vessels.

Restoration of flow-dependent coronary artery dilation by angiotensin-converting enzyme inhibition (ACEI) has been demonstrated in patients with hypertension. The aim of the present study was to evaluate whether dilation of conductance coronary arteries may alter maximal coronary blood flow (CBFmax) and minimal coronary resistance (CRmin) in hypertensive patients with reversible impairment of flow-dependent coronary artery dilation. Thirteen hypertensive patients with angiographically normal coronary arteries and no other risk factors were studied. Cross-sectional areas (CSAs) of proximal and distal left anterior descending (LAD) coronary arteries were determined by quantitative angiography. Coronary flow velocity was recorded in the distal LAD with an intracoronary Doppler catheter. Estimates of coronary blood flow and resistance were calculated at rest and during maximal increase in blood flow induced by papaverine injected in the midportion of the LAD, both before and after ACEI. Flow-dependent dilation of the proximal LAD, abolished before ACEI, was restored after (26.7 +/- 11.2%; p < 0.001). The increase in CSA of the distal LAD exposed to papaverine was significantly higher after ACEI than before (from 33.4 +/- 20.5% to 51.5 +/- 23.4%; p < 0.001). After restoration of proximal LAD flow-dependent dilation, CBFmax was increased by +21.0 +/- 10.3% (p < 0.001), and CRmin was reduced by 19.3 +/- 9.5% (p < 0.001). Thus, dilation of epicardial coronary arteries participates substantially in the coronary resistance in hypertensive patients. Restoration of flow-dependent coronary artery dilation by ACEI may improve the ability of coronary circulation to deliver its maximal myocardial blood flow in hypertensive patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

[Dysfunction of the coronary microcirculation in type 2 diabetic patients].

A failure of coronary blood flow to increase during cold pressor test has been shown in patients with coronary atherosclerosis and impaired metabolic coronary vasodilatation in response to atrial pacing has been demonstrated in diabetic patients without significant epicardial artery stenoses. This study was designed to evaluate coronary microvascular adaptation to increased myocardial oxygen demand in response to sympathetic stimulation in diabetic patients with angiographically normal coronary arteries. Microvascular coronary adaptation to increased myocardial oxygen demand due to sympathetic stimulation evoked by the cold pressor test has been examined in 22 type 2 diabetic patients and in 15 control subjects with angiographically normal coronary arteries and no other risk factors. Coronary blood flow was calculated by measuring mean flow velocity in left anterior descending coronary artery by intracoronary Doppler and cross sectional area of the artery by digital angiography. Results show that despite a similar increase in rate-pressure product in the 2 groups (+22.6 +/- 12.4% in diabetic patients and +31.8 +/- 8.2% in control subjects, NS), coronary blood flow increase in left anterior descending artery was significantly lower in diabetic patients than in control subjects (+14.7 +/- 19.8% vs +75.5 +/- 13.5%, respectively, p = 0.0001). In addition, when there was a positive correlation between the 2 parameters in control subjects (R = 0.651, p < 0.01), there was no relationship in diabetic patients (R = 0.054). In conclusion, this study demonstrates that vasodilatation of coronary microcirculation in response to sympathetic stimulation evoked by cold pressor test is impaired in type 2 diabetic patients without epicardial artery lesions. This microvascular impairment during sympathetic stimulation may explain exercise-induced myocardial perfusion abnormalities observed in these patients and may impair microcirculatory coronary vasodilatation during current life stress episodes such as exercise, mental stress or cold exposure.

Adaptation, Physiological↗
PubMed1999

Effects of nicotine gum on coronary vasomotor responses during sympathetic stimulation in patients with coronary artery stenosis.

Smoking-cessation rates may be improved by nicotine-replacement therapy that reduces withdrawal symptoms. However, nicotine may have adverse effects on coronary circulation. The purpose of this study was to examine the short-term effects of nicotine gum chewing on the dimensions of coronary arteries of patients with coronary artery disease and on the response of coronary vessels to sympathetic stimulation caused by the cold pressor test. In 17 patients who were past chronic cigarette smokers, cross-sectional areas of 32 coronary artery stenoses and 32 adjacent apparently normal segments were measured by using quantitative coronary angiography at baseline and after a cold pressor test before and after nicotine gum chewing. The cold pressor test produces an increase in arterial pressure without any change in heart rate. These changes were similar before and after nicotine gum. Before nicotine gum, the cross-sectional area of coronary stenoses and apparently normal segments was significantly and similarly reduced during the cold pressor test (-11+/-12% and -11+/-12%, respectively; both p values <0.0001 vs. baseline). After nicotine gum, baseline cross-sectional area was not modified, and response to the cold pressor test was similar to that observed before nicotine gum (-11+/-18% and -12+/-12%, respectively; both p values <0.0001 vs. baseline). In conclusion, nicotine-replacement therapy by using nicotine gum does not reduce the surface area of normal and diseased coronary segments and does not enhance the constricting effect of sympathetic stimulation produced by the cold pressor test. Thus nicotine gum may be considered a relatively safe drug in patients who need nicotine-replacement therapy to stop smoking.

Administration, Oral↗
PubMed1999

[Left ventricular performance, ventriculo-arterial coupling and mechanical output in hypertensive patients with and without left ventricular hypertrophy].

Left ventricular hypertrophy (LVH) is a physiological process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular (LV) contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in hypertensive patients with LVH. To assess the differences between patients with and without LVH, LV contractile performance, the ventriculoarterial coupling and mechanical efficiency were compared in 2 groups of hypertensive patients with similar body surface area and arterial pressures, 23 without LVH (group 1) and 30 with LVH (group 2) and compared to data of 20 normotensive subjects. Left ventricular angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Left ventricular contractile performance assessed by Ees/100 g myocardial mass and EESVR were lower in group 2 than in group 1 (1.23 +/- 0.28 vs 1.89 +/- 0.48 mmHg/mL/100 g and 6.22 +/- 1.07 vs 9.56 +/- 0.97 g/cm2/mL/m2, respectively, both p < 0.0001, control subjects: 1.47 +/- 0.41 and 6.97 +/- 1.22, respectively). Ventriculoarterial coupling evaluated through Ea/Ees ratio (0.51 +/- 0.05 in group 1 vs 0.53 +/- 0.08 in group 2, 0.49 +/- 0.09 in control subjects), and work efficiency evaluated through EW/PVA ratio (0.80 +/- 0.02 in group 1 vs 0.78 +/- 0.03 in group 2, 0.80 +/- 0.03 in control subjects), were similar in the 2 groups and were comparable to control subject values. In conclusion, this study shows that ventriculoarterial coupling and work efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in patients without LVH the matching between left ventricle and arterial receptor is preserved through an enhancement of myocardial contractility which is energetically costly. Conversely, LVH seems to be a useful adaptation which minimizes the energetical cost of high pressure generation.

Biomechanical Phenomena↗
PubMed1998

Left ventricular contractile performance, ventriculoarterial coupling, and left ventricular efficiency in hypertensive patients with left ventricular hypertrophy.

Contractile performance of hypertrophied left ventricle may be depressed in arterial hypertension. Ventriculoarterial coupling is impaired when myocardial contractile performance is reduced and when afterload is increased. The left ventricular contractile performance and the ventriculoarterial coupling were evaluated in 30 hypertensive patients with moderate left ventricular hypertrophy and 20 control subjects. Left ventricular angiography coupled with the simultaneous recording of pressures with a micromanometer were used to determine end-systolic stress/volume index, the slope of end-systolic pressure-volume relationship, ie, end-systolic elastance, effective arterial elastance, external work, and pressure-volume area. In hypertensive patients, left ventricular contractile performance, as assessed by end-systolic elastance/ 100 g myocardial mass, was depressed (4.35 +/- 1.13 v 5.21 +/- 1.89 mm Hg/mL/100 g in control subjects P < .02), when end-systolic stress-to-volume ratio was comparable in the two groups (3.85 +/- 0.99 g/cm2/mL in hypertensive patients versus 3.51 +/- 0.77 g/cm2/mL in control subjects). Ventriculoarterial coupling, evaluated through effective arterial elastance/end-systolic elastance ratio, was slightly higher in hypertensive patients (0.53 +/- 0.08 v 0.48 +/- 0.09 mm Hg/mL in control subjects, P < .05), and work efficiency (external work/pressure-volume area) was similar in the two groups (0.78 +/- 0.04 mm Hg/mL in hypertensive patients versus 0.80 +/- 0.03 mm Hg/mL in control subjects). This study shows that despite a slight depression of left ventricular contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in hypertensive patients with left ventricular hypertrophy. Thus, it appears that left ventricular hypertrophy might be a useful means of preserving the match between left ventricle and arterial receptor with minimal energy cost.

Arteries↗
PubMed1998

Acute effects of angiotensin-converting enzyme inhibition on coronary vasomotion in hypertensive patients.

Coronary vasodilator responses to pharmacological (acetylcholine) and physiological (cold pressor test and flow dependent dilation) stimuli are impaired in hypertensive patients. The ability of angiotensin-converting enzyme inhibitors to restore normal coronary responses in hypertension and the potential mechanisms involved are examined. In spontaneously hypertensive rats, angiotensin-converting enzyme inhibitors prevent impairment of endothelial-dependent relaxation of arterial rings in response to acetylcholine; in dogs, intracoronary infusion of an angiotensin-converting enzyme inhibitor dilates epicardial arteries and enhances coronary blood flow. In hypertensive patients with normal coronary arteries, intravenous administration of the angiotensin-converting enzyme inhibitor perindoprilat changes constriction of coronary arteries to dilation in response to the cold pressor test, and the absence of flow-dependent dilation becomes a normal response. In addition, maximal coronary blood flow induced by papaverine is enhanced by angiotensin-converting enzyme inhibition and minimal coronary resistance is reduced. It is concluded that both animal and human studies have demonstrated that angiotensin-converting enzyme inhibitors may acutely reverse the abnormalities of coronary vasomotion in arterial hypertension. However, not all the mechanisms responsible are fully understood and further studies are needed, particularly to determine the exact role of nitric oxide, bradykinin and oxygen-derived free radicals.

Angiotensin-Converting Enzyme Inhibitors↗
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

[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↗