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Biomedical subjects

J Mayet

Publications and source records attributed to J Mayet.

At least 37 records · Page 2Linked to original sources

Effects of blood pressure lowering with amlodipine or lisinopril on vascular structure of the common carotid artery.

Increased intima-media thickness of the common carotid artery predicts increased risk of myocardial infarction and stroke. Preliminary evidence suggests that a decrease in blood pressure (BP) is associated with diminished wall thickness. It is not known if all classes of anti-hypertensive agents have similar protective effects. In this double-blind parallel-group clinical trial, 69 previously untreated patients with hypertension were allocated randomly to 1 year of treatment with either amlodipine (5-10 mg daily) or lisinopril (5-20 mg daily). Doxazosin and bendrofluazide were added if required to achieve BP control. After 12 months of treatment, clinic BP, ambulatory BP and cardiac mass were reduced similarly by the two treatment regimens. Common carotid artery intima-media thickness decreased by 0.048 mm (95% confidence intervals -0.066, -0.031 mm) in the amlodipine-treated group, but decreased by only 0.027 mm (-0.046, -0.007 mm) in the lisinopril-treated group (P<0.05 for difference between treatments). Common carotid artery lumen diameter declined significantly only in patients treated with lisinopril [amlodipine, -0.02 mm (-0.14, 0.10 mm); lisinopril, -0.21 mm (-0.32, -0.11 mm); P<0.02], while intima-media area declined similarly in the two treatment groups [amlodipine -1.32 mm(2) (-1.91, -0.74 mm(2)), lisinopril -1.26 mm(2) (-1.80, -0.72 mm(2)); not significant]. The results confirm that a decrease in BP causes regression of structural changes in the carotid artery in hypertensive patients. The nature of the structural regression differed markedly between the two treatment regimens, in spite of similar decreases in BP. The calcium channel blocker induced greater regression of common carotid artery intima-media thickness than the angiotensin-converting enzyme inhibitor. However, carotid artery wall mass, as indicated by intima-media area, was reduced to a similar extent by the two treatments. It remains to be established whether such differences confer a prognostic advantage.

Adult↗

Absence of sympathetic overactivity in Afro-Caribbean hypertensive subjects studied by heart rate variability.

Black hypertensives present a greater prevalence of left ventricular hypertrophy and an increased mortality compared to white hypertensives. Differences in sympathetic activity might contribute to explain these racial differences in hypertension. Nevertheless, previous laboratory studies did not show any increase of sympathetic activity direct to the heart in black subjects. The aim of the present study was to investigate the cardiac sympatho-vagal balance in black and white hypertensives analysing heart rate variability, during the entire 24 h. We analysed Holter recordings of 52 essential hypertensive patients, who had never received antihypertensive treatment, 26 of whom were black and 26 were white. Consecutive series of 300 beats, with 150 beats overlapped (approximately 600 series/day), were considered for the analysis in time and frequency domain. The mean 24-h value of the power of the low frequency spectral component (0.04-0.15 Hz), expressed in normalised units, ie a marker of sympathetic modulation, was significantly lower in the group of black patients compared to whites (respectively 40.0 +/- 2.1 vs 53.6 +/- 3.6 nu, P < 0.01). Similar results were observed for the LF/HF ratio, an index of the sympatho-vagal balance (respectively 4.11 +/- 0.58 vs 5.98 +/- 0.79; P < 0.05). In a multiple linear regression analysis, considering diastolic blood pressure, left ventricular mass index, race and age as independent variables, only race (P < 0.002) and age (P < 0.01) could independently predict the normalised low frequency power or the LF/HF ratio, as dependent variables. The results of this study suggest some blunting of the cardiac sympathetic neural modulation in black hypertensives compared to white hypertensives, during the entire 24 h.

Adult↗

Stress echocardiography for the diagnosis of ischaemia in hypertensives.

Exercise treadmill electrocardiography and myocardial perfusion imaging are commonly used in non-invasive tests for the detection of myocardial ischaemia. Unfortunately there are limitations in the assessment of hypertensive patients since these tests frequently provide false-positive results, particularly in those subjects with left ventricular hypertrophy. In order to investigate the utility of stress echocardiography in hypertensive patients we assessed 173 subjects undergoing this investigation in our department. Of these, 66 had had coronary angiography within 6 months. Thirty subjects were hypertensives, 17 with left ventricular hypertrophy, and 36 normotensives. Patients with a 70% or greater stenosis at coronary angiography were deemed to have sufficient disease to cause myocardial ischaemia. The overall sensitivity of stress echocardiography for detecting myocardial ischaemia was 83% with a specificity of 77%. For the hypertensive group alone the sensitivity was 93% and specificity 73%. The normotensives had a sensitivity of 76% with a specificity of 80%. In conclusion, in this group of hypertensives stress echocardiography had a favourable specificity and this was not significantly different from that of normotensive subjects. Journal of Human Hypertension (2000) 14, 399-401

Coronary Angiography↗

Ethnic and gender differences in electrocardiographic QT length and QT dispersion in hypertensive subjects.

BACKGROUND: Prolonged QT intervals and/or increased QT dispersion (QTd) are associated with various pathological conditions and predict death in healthy individuals. Among hypertensives, QTd correlates with blood pressure (BP) and left ventricular mass index (LVMI) and QT intervals are prolonged in those with left ventricular hypertrophy (LVH). In normotensives, heart-rate corrected QT length (QTc) is longer in females than males, but QTd is greater in males than females. There are few data comparing QT parameters between different ethnic groups and none specifically in hypertensives. Among normotensives, compared with whites, QTc is reported to be shorter in African-Americans and longer in Chinese. We looked for ethnic and gender differences in QT parameters in hypertensive subjects. METHODS: Untreated hypertensives were selected from a Hypertension Clinic database. Black and white subjects were matched for age, sex, BP and LVMI. Male and female subjects were matched for age, race, BP and the presence or absence of echocardiographic LVH. Maximum QT intervals (QTm), rate-corrected maximum QT intervals (QTc) and QT dispersion (QTd) were measured or calculated from ECGs. Data are presented as mean +/- s.d. Differences in QT parameters were sought between groups using Student's t-tests. RESULTS: No ethnic or gender differences in QT parameters achieved statistical significance. However there was a tendency for QTm and QTc to be prolonged in blacks compared with whites (443 +/- 52 vs 421 +/- 47; P = 0.08 and 480 +/- 65 vs 463 +/- 40: P = 0.24 respectively), and for QTc to be prolonged in females compared with males (479 +/- 52 vs 461 +/- 45 ms; P= 0.13). CONCLUSION: In small groups of matched hypertensives, no ethnic or gender differences in QT parameters achieved statistical significance. However, similar to findings in normotensives, QTc tended to be longer in hypertensive females than males. In hypertensives, we failed to confirm the finding that QTc is shorter in blacks than whites, as seen in US normotensives. Whether this represents a difference between hypertensives and normotensives, or between US and UK blacks requires further investigation. Whether the prognostic significance of QT parameters in hypertensives differs between different gender and ethnic groups needs to be established from prospective studies. Journal of Human Hypertension (2000) 14, 403-405

Adult↗

Improvement in midwall myocardial shortening with regression of left ventricular hypertrophy.

Despite normal indices of left ventricular (LV) chamber function, patients with LV hypertrophy (LVH) due to hypertension are thought to have depressed midwall systolic shortening compared with normotensives. The aims of the present study were (1) to confirm this observation and (2) to assess the effects of antihypertensive therapy that cause regression of LVH on LV systolic function assessed at both the midwall and endocardium. Thirty-eight previously untreated hypertensive subjects with LVH underwent echocardiography and were compared with 38 normotensive control subjects. Comparisons between the group with LVH and the control group revealed no significant differences in cardiac output (4. 32+/-0.23 versus 4.55+/-0.21 L/min), ejection fraction (62.5+/-2% versus 66.4+/-1.07%), or endocardial fractional shortening (34.5+/-1.45% versus 37.0+/-0.82%), but shortening assessed at the midwall was significantly less in the group with LVH (17.9+/-1.11% versus 21.6+/-0.63%, P<0.01). Subsequently, 32 patients with uncontrolled hypertension (24 previously untreated and 8 on existing antihypertensive therapy) underwent treatment with ramipril, with the addition of felodipine and bendrofluazide if required, to reduce blood pressure to <140/90 mm Hg. These 32 patients underwent echocardiography at baseline, after blood pressure control, and after an additional 6 months of tight blood pressure control. Good blood pressure control was achieved after 6 months compared with baseline (143/86+/-2.8/1.4 versus 174/103+/-4.1/1.9 mm Hg; P<0.01) with significant regression of LV mass index (124+/-3.4 versus 145+/-3.8 g/m(2), P<0.01). LV fractional shortening assessed at the midwall improved with regression of LVH (21.9+/-0.84 and 18.7+/-1. 19%, P<0.05), with posttreatment midwall shortening being similar to that of the normal control subjects evaluated in the first study. Hypertensive patients with LVH have depressed midwall systolic shortening despite normal indices of LV chamber function. Regression of LVH after good blood pressure control improved midwall shortening to normal levels.

Adult↗

Effects of 7 years of growth hormone replacement therapy in hypopituitary adults.

Short-term studies of GH replacement in adult hypopituitarism have usually demonstrated beneficial effects on body composition and circulating lipids, with neutral or occasionally adverse effects on glucose tolerance. Fasting hyperinsulinemia has been reported. GH effects on cardiac function have been variable. The effects of long-term GH therapy, taking into account the consequences of increasing age, are not fully known. Thirty-three hypopituitary, initially middle-aged adults were studied over a 7-yr period; 12 patients took GH therapy (mean, 0.7 mg daily) continuously (group A); 11 took GH for only 6-18 months, a minimum of 5 yr previously (group B); and 10 patients never received GH therapy (group C). Other pituitary replacement was maintained. Effects on anthropometry, body composition (by bioimpedance analysis, total body potassium, and dual energy x-ray absorptiometry), circulating lipids, glucose and insulin concentrations, cardiac 2-dimensional and Doppler echocardiography, and exercise tolerance were assessed before and after the treatment period. Continuous GH therapy had no significant effect on body weight, but it prevented the increase in waist circumference and waist to hip ratio that occurred in the patients without GH substitution (waist to hip ratio, group A, 0.87+/-0.08 at baseline, 0.85+/-0.09 at 7 yr; group B, 0.89+/-0.11 at baseline, 0.94+/-0.11 at 7 yr; P < 0.005 for GH effect; group C, 0.87+/-0.10 at baseline, 0.92+/-0.10 at 7 yr; P < 0.005 for GH effect). A GH-induced decrease in subscapular skinfold thickness was also observed. By bioimpedance analysis, GH therapy caused an increase in total body water and fat-free mass, and a decrease in the percent body fat. Although changes occurred with time in all groups, no significant additional GH therapy effects were observed on glucose tolerance, insulin concentrations, lipid levels, cardiac dimensions, echocardiographic diastolic function, or exercise tolerance. In conclusion, prolonged GH substitution in middle-aged hypopituitary adults causes a sustained improvement in body composition. Other benefits, e.g. on lipid levels and exercise tolerance, were not apparent at 7 yr when comparisons were made with GH-untreated hypopituitary controls. Potentially adverse effects on glucose tolerance and insulinemia did not develop with prolonged GH therapy.

Absorptiometry, Photon↗

QT dispersion in athletic left ventricular hypertrophy.

OBJECTIVE: To assess whether physiologic left ventricular hypertrophy as a result of physical training is associated with an increased QT length or dispersion. METHODS: Thirty-three subjects were assessed. These consisted of a group of international endurance athletes (including 8 rowers, 2 cyclists, and 1 triathlete), a group of 12 professional soccer players, and a further group of 10 control subjects. Each underwent 2-dimensional echocardiography and 12-lead electrocardiographic examination. RESULTS: Left ventricular mass index was considerably greater in both the endurance athlete (163.3 +/- 14.4 g/m2; P <.01) and soccer player groups (144.2 +/- 5.5 g/m 2; P <.05) compared with the controls (109.2 +/- 6.3 g/m2). In spite of these large differences in cardiac structure there were no significant differences in QT parameters between the groups (QT dispersion 56.9 +/- 5.5, 68.5 +/- 9.5, and 67.2 +/- 12.6 ms; QTc dispersion 61.4 +/- 9.2, 69.4 +/- 13.3, and 54.2 +/- 6.5 ms; maximum QT 402 +/- 10.3, 404 +/- 9.6, and 392 +/- 14.0 ms; and maximum QTc 404 +/- 7.0, 413 +/- 9.3, and 399 +/- 9.9 ms among endurance athletes, soccer players, and controls, respectively). CONCLUSION: Left ventricular hypertrophy occurring as a consequence of athletic training does not appear to be associated with a major increase in QT length or QT dispersion.

Adult↗

Ethnic differences in the identification of left ventricular hypertrophy in the hypertensive patient.

Left ventricular hypertrophy (LVH) is more prevalent in black than white hypertensives, but this difference is greater when identified by electrocardiography (ECG) than by echocardiography. We evaluated the proposal that current ECG criteria for LVH are less specific, and therefore, less useful, in blacks than whites. In a retrospective cross-sectional study, 408 subjects (271 white, 137 black) referred to a hypertension clinic for assessment of hypertension underwent measurement of blood pressure, ECG voltages (Sokolow-Lyon and Cornell sex-specific), and echocardiographic left ventricular mass index (LVMI). Black subjects had greater ECG voltages than whites, even when closely matched for LVMI. In black subjects, current ECG criteria were twice as sensitive as in whites (Sokolow-Lyon: 44.9% v 22.5%, P = .003. Cornell: 30.4% v 15.7%, P = .03). They were less specific in blacks using the Sokolow-Lyon criteria (73.5% v 86.8%, P = .02) but this failed to reach significance using the Cornell criteria (83.8% v 91.8%, P = .07). When voltage criteria were adjusted to give matched sensitivities and specificities, respectively, differences in specificity and sensitivity were no longer apparent. Receiver operating characteristic curve analyses confirmed no significant differences in overall performance of either ECG criteria between blacks and whites. In conclusion, ECG detection of LVH is insensitive in both ethnic groups. Sensitivity is higher in blacks due to higher LVMI in those with LVH. Apparent differences in specificity are due to ethnic differences in ECG voltages that are unrelated to differences in LVMI. When these differences are taken into account, there are no overall differences in test accuracy. However, given the prognostic importance of the detection of LVH, currently accepted ECG voltage criteria for the detection of LVH remain of equal or greater value in black hypertensives compared with whites.

Adult↗

Intraventricular dispersion of E wave velocity: an alternative measure of left ventricular diastolic function in hypertensive patients?

The E/A ratio (of peak mitral blood flow velocity during early diastole to that during atrial contraction) has limitations in the assessment of diastolic function. Previous studies have suggested that peak blood flow velocity is normally maintained or increased towards the cardiac apex but that it decreases in diastolic dysfunction. We evaluated the proposal that intraventricular dispersion of E wave velocity is an effective means of assessing diastolic function in hypertensives. Fifty-five untreated hypertensive patients underwent echocardiographic examination. Pulsed-wave Doppler recordings were made from the apical four-chamber view. Peak flow velocities were measured during early diastole at the level of the mitral valve (E0), and 3 cm distally (E3), and during atrial contraction at the level of the mitral valve (A). Mean peak flow velocities were 64.4 +/- 16.1 m/s for E0, 50.6 +/- 17.9 m/s for E3 and 61.1 +/- 12.1 m/s for A. Peak flow velocity during early diastole slowed towards the cardiac apex in most patients (E3/E0 range: 0.42-1.86, mean 0.81 +/- 0.29). There was no significant difference in E3/E0 between those with and without left ventricular hypertrophy (LVH) (0.76 +/- 0.25 vs 0.82 +/- 0.29, P = 0. 39). E3/E0 did not correlate with age (r = -0.02, P = 0.89), systolic blood pressure (BP) (r = 0.17, P = 0.20), diastolic BP (r = 0.21, P = 0.12) or LVMI (r = -0.11, P = 0.40). In contrast the E/A ratio correlated strongly with age (r = -0.66, P < 0.0001) and negatively, though not significantly, with systolic BP (r = -0.24, P = 0.07), diastolic BP (r = -0.23, P = 0.09) and LVMI (r = -0.23, P = 0.08). Although there is some intraventricular dispersion of E wave velocity in this group of hypertensive patients, the ratio of E3/E0 correlates poorly with parameters which are known to influence diastolic function. In spite of its limitations, the E/A ratio appears to be a more reliable measure of diastolic function in hypertensive heart disease than intraventricular dispersion of early diastolic filling.

Adult↗

Anticoagulation for cardioversion of atrial arrhythmias.

We would advocate 3 weeks of anticoagulation prior to, and 4 weeks post-cardioversion (either electrical or chemical) for patients in chronic atrial fibrillation or flutter. In selected cases it seems reasonable to use transoesophageal echocardiography to exclude preformed thrombus and negate the need for 3 weeks of prior anticoagulation. For patients presenting acutely with atrial fibrillation or flutter we suggest anticoagulating with heparin immediately on presentation and for those who do not spontaneously revert to sinus rhythm, using transoesophageal echocardiography to exclude atrial thrombi prior to cardioversion. Oral anticoagulation should be continued for 4 weeks post-procedure. If transoesophageal echocardiography is not readily available an alternative strategy would be to anticoagulate the patient for 3 weeks and thereafter readmit them for elective cardioversion, continuing the anticoagulation for a further 4 weeks after the procedure.

Acute Disease↗

Ethnic differences in the hypertensive heart and 24-hour blood pressure profile.

Black hypertensive persons have been observed to have a greater degree of left ventricular hypertrophy than white hypertensives. However, previous studies have matched groups for blood pressure (BP) measured in the clinic, and it has been demonstrated that black hypertensives have an attenuated nocturnal BP dip. Clinic BPs may thus underestimate mean 24-hour BP in this group. To investigate whether the differences in left ventricular hypertrophy can be accounted for by the greater mean 24-hour BP in black hypertensives, 92 previously untreated hypertensives were studied with 24-hour ambulatory BP monitoring and echocardiography. The 46 black hypertensives (24 men and 22 women) were matched with the 46 white hypertensives for age, gender, and mean 24-hour BP. Despite similar mean 24-hour BPs (blacks, 142/93 mm Hg; whites, 145/92 mm Hg; P=.53/.66), the black group had a smaller mean nocturnal dip than the white group (blacks, 8/8 mm Hg; whites, 16/13 mm Hg; P<.01). In addition, mean left ventricular mass index (LVMI) was greater (blacks, 130 g/m2; whites, 107 g/m2; P<.001). Mean 24-hour systolic BP was significantly related to LVMI in both groups (blacks, r=.45, P<.01; whites, r=.56, P<.01). However, systolic BP dip correlated inversely with LVMI only in the black group (blacks, r=-.30, P<.04; whites, r=.05, P=.76). In a multiple regression model, LVMI was independently related to both mean daytime BP and mean nocturnal BP dip in black subjects but only to mean daytime BP in white subjects. In conclusion, the increased left ventricular hypertrophy observed in black hypertensives compared with white hypertensives is not accounted for by differences in mean 24-hour BP. However, LVMI in black hypertensives appears to be more dependent on nocturnal BP than that in white hypertensives; this, coupled with the attenuated BP dip in black hypertensives, suggests that the BP profile rather than 24-hour BP may be important in determining the differences in left ventricular hypertrophy.

Adult↗