Ethnic differences in cross-sectional associations between impaired glucose regulation, identified by oral glucose tolerance test or HbA1c values, and cardiovascular disease in a cohort of European and South Asian origin.

AIMS: We contrasted impaired glucose regulation (prediabetes) prevalence, defined according to oral glucose tolerance test or HbA1c values, and studied cross-sectional associations between prediabetes and subclinical/clinical cardiovascular disease (CVD) in a cohort of European and South Asian origin. METHODS: For 682 European and 520 South Asian men and women, aged 58-85 years, glycaemic status was determined by oral glucose tolerance test or HbA1c thresholds. Questionnaires, record review, coronary artery calcification scores and cerebral magnetic resonance imaging established clinical plus subclinical coronary heart and cerebrovascular disease. RESULTS: Prediabetes was more prevalent in South Asian participants when defined by HbA1c rather than by oral glucose tolerance test criteria. Accounting for age, sex, smoking, systolic blood pressure, triglycerides and waist-hip ratio, prediabetes was associated with coronary heart disease and cerebrovascular disease in European participants, most obviously when defined by HbA1c rather than by oral glucose tolerance test [odds ratios for HbA1c -defined prediabetes 1.60 (95% CI 1.07, 2.39) for coronary heart disease and 1.57 (95% CI 1.00, 2.51) for cerebrovascular disease]. By contrast, non-significant associations were present between oral glucose tolerance test-defined prediabetes only and coronary heart disease [odds ratio 1.41 (95% CI 0.84, 2.36)] and HbA1c -defined prediabetes only and cerebrovascular disease [odds ratio 1.39 (95% CI 0.69, 2.78)] in South Asian participants. Prediabetes defined by HbA1c or oral glucose tolerance test criteria was associated with cardiovascular disease (defined as coronary heart and/or cerebrovascular disease) in Europeans [odds ratio 1.95 (95% CI 1.31, 2.91) for HbA1c prediabetes criteria] but not in South Asian participants [odds ratio 1.00 (95% CI 0.62, 2.66); ethnicity interaction P = 0.04]. CONCLUSIONS: Prediabetes appeared to be less associated with cardiovascular disease in the South Asian than in the European group. These findings have implications for screening, and early cardiovascular prevention strategies in South Asian populations.

Platelet and leukocyte activation, atherosclerosis and inflammation in European and South Asian men.

BACKGROUND: Increased platelet activation occurs in ischemic heart disease (IHD), but increased platelet activation is also seen in cerebrovascular atherosclerosis and peripheral artery disease. It is not clear therefore whether platelet activation is an indicator of IHD or a marker of generalized atherosclerosis and inflammation. South Asian subjects are at high risk of IHD, but little is known regarding differences in platelet and leukocyte function between European and South Asian subjects. METHODS: Fifty-four male subjects (age 49-79 years) had coronary artery calcification measured by multislice computed tomography (CT), aortic atherosclerosis assessed by measurement of carotid-femoral pulse wave velocity (aortic PWV), and femoral and carotid atherosclerosis measured by B-mode ultrasound. Platelet and leukocyte activation was assessed by flow cytometry of platelet-monocyte complexes (PMC), platelet expression of PAC-1 binding site and CD62P, and expression of L-selectin on leukocytes. RESULTS: Elevated circulating PMC correlated significantly with elevated aortic PWV and PMC were higher in subjects with femoral plaques. In contrast PMC did not differ by increasing coronary artery calcification category or presence of carotid plaques. Higher numbers of PMC were independently related to elevated levels of C-reactive protein (CRP), higher aortic PWV, hypertension and smoking in a multivariate model. Markers of platelet and leukocyte activation did not differ significantly by ethnicity. CONCLUSIONS: Increased PMC are related to the extent of aortic and femoral atherosclerosis rather than coronary or carotid atherosclerosis. The association between elevated CRP and increased PMC suggests that inflammation in relation to generalized atherosclerosis may play an important role in PMC activation.

The Coronary Artery Revascularisation in Diabetes (CARDia) trial: background, aims, and design.

BACKGROUND: Patients with diabetes have an increased incidence and severity of ischemic heart disease, which leads to an increased requirement for coronary revascularization. Comparative information regarding mode of revascularization--coronary artery bypass graft surgery surgery (CABG) or percutaneous coronary intervention (PCI)--is limited, mainly confined to a subanalysis of the Bypass Angioplasty Revascularization (BARI) trial, suggesting a mortality benefit of CABG over PCI. No prospective trial has specifically compared these modes of revascularization in patients with diabetes. OBJECTIVE: The Coronary Artery Revascularisation in Diabetes (CARDia) trial is designed to address the hypothesis that optimal PCI is not inferior to modern CABG as a revascularization strategy for diabetics with multivessel or complex single-vessel coronary disease. The primary end point is a composite of death, nonfatal myocardial infarction, and cerebrovascular accident at 1 year. METHOD: A total of 600 patients with diabetes are to be randomized to either PCI or CABG, with few protocol restrictions on operative techniques or use of new technology. This gives a power of 80% to detect non-inferiority of PCI assuming that the PCI 1-year event rate is 9%. A cardiac surgeon and a cardiologist must agree that a patient is suitable for revascularization by either technique prior to recruitment into the study. Twenty-one centers in the United Kingdom and Ireland are recruiting patients. Data on cost effectiveness, quality of life, and neurocognitive function are being collected. Long-term (3-5 year) follow-up data will also be collected.

Echocardiographic methods for selecting patients suitable for biventricular pacing therapy.

The large outcome studies of biventricular pacing to date have selected patients using electrocardiogram criteria (prolonged QRS and left bundle branch block morphology). However, 20-30% of patients do not appear to respond clinically, and as a result there has been much interest in developing more specific methods of detecting mechanical dyssynchrony. A number of different echocardiographic techniques have been developed which appear to offer greater sensitivity and specificity than ECG in selecting these patients. This paper reviews the most promising of the echocardiographic techniques and gives guidance for the clinical use of echocardiography in selecting patients for biventricular pacing.

The effects of antihypertensive therapy on carotid vascular structure in man.

OBJECTIVE: An increased carotid intima-media thickness (IMT) has been found to be associated with a number of cardiovascular risk factors such as age, hypertension, cigarette smoking, hypercholesterolaemia and left ventricular hypertrophy. Our objective was to assess whether carotid intima-media thickness in hypertensive patients could be reduced by antihypertensive therapy. METHODS: 13 hypertensive patients, 10 previously untreated, were examined using carotid ultrasonography and echocardiography at baseline and then at 8 weeks and 39 weeks after commencement of antihypertensive therapy with ramipril and the second-line addition of felodipine. RESULTS: By the end of the study significant regression of IMT (0.1(0.05-0.16) mm, F-value 10.2, P < 0.01) and left ventricular mass index had occurred (25(10.7-39.3) g/m2, F-value 9.7, P < 0.01). The reduction in IMT was significantly related to the reduction in mean arterial pressure, r = 0.55, P = 0.05). CONCLUSION: Antihypertensive therapy with ramipril and felodipine causes regression of IMT in hypertensive patients, probably chiefly through blood pressure reduction. Large prospective studies are required to assess whether a reduction in IMT results in a reduction in morbidity and mortality.

Left ventricular hypertrophy and QT dispersion in hypertension.

The interlead variation in QT length on a standard electrocardiograph reflects regional repolarization differences in the heart. To investigate the association between this interlead variation (QT dispersion) and left ventricular hypertrophy, we subjected 100 untreated subjects to 12-lead electrocardiography and echocardiography. Additionally, 24 previously untreated subjects underwent a 6-month treatment study with ramipril and felodipine. In the cross-sectional part of the study, QT dispersion corrected for heart rate (QTc dispersion) was significantly correlated with left ventricular mass index (r = .30, P < .01), systolic pressure (r = .30, P < .01), the ratio of peak flow velocity of the early filling wave to peak flow velocity of the atrial wave (E/A ratio) (r = -.22, P = .02), isovolumic relaxation time (r = .31, P < .01), and age (r = .21, P < .04). In the treatment part of the study, lead-adjusted QTc dispersion decreased from 24 to 19 milliseconds after treatment, and after a subsequent 2 weeks of drug washout remained at 19 milliseconds (P < .01). The changes in left ventricular mass index at these stages were 144, 121, and 124 g/m2 (P < .01). Systolic pressure decreased from 175 to 144 mm Hg and increased again to 164 mm Hg after drug washout (P < .01). The E/A ratio (0.97, 1.02, and 1.02; P = 69) and isovolumic relaxation time (111, 112, and 112; P = .97) remained unchanged through the three assessment points. In conclusion, QT dispersion is increased in association with an increased left ventricular mass index in hypertensive individuals. Antihypertensive therapy with ramipril and felodipine reduced both parameters. If an increased QT dispersion is a predictor of sudden death in this group of individuals, then the importance of its reduction is evident.

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.

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.

Ventricular arrhythmias in hypertension: in which patients do they occur?

OBJECTIVE: It has been suggested that the increased incidence of sudden death in hypertensive patients, particularly those with left ventricular hypertrophy, may be casually related to the increased number and complexity of ventricular arrhythmias that have been demonstrated in these patients. The objective of the present study was to assess some of the factors which might be responsible for these arrhythmias. SUBJECTS AND METHODS: One hundred and three untreated subjects were divided into four groups on the basis of blood pressure and echocardiographic measurements: hypertensive patients with left ventricular hypertrophy (n = 38), hypertensive patients without left ventricular hypertrophy (n = 16), patients with borderline or white-coat hypertension (n = 26) and normotensive subjects (n = 23). Each subject underwent two-dimensional and Doppler echocardiography, 12-lead electrocardiogram examination, 12-lead electrocardiogram exercise stress testing, 24-h ambulatory blood pressure monitoring and 24-h Holter monitoring. A further 17 hypertensive patients with left ventricular hypertrophy who were on long-term antihypertensive therapy were also investigated in the same manner and compared with untreated hypertensive patients with left ventricular hypertrophy who were matched for age, sex and race. RESULTS: Untreated hypertensive patients, even with left ventricular hypertrophy, had a low prevalence of frequent or complex arrhythmias (seven out of 80 patients with Lown score 2+). In contrast, hypertensive patients with left ventricular hypertrophy on long-term antihypertensive therapy had a significantly greater prevalence of complex arrhythmias than untreated patients with left ventricular hypertrophy (eight out of 17 treated patients compared with two out of 17 untreated patients with Lown score 2+). CONCLUSIONS: Hypertensive patients with left ventricular hypertrophy who had received long-term antihypertensive therapy were found to have a high prevalence of complex ventricular arrhythmias, which was in contrast to untreated hypertensive patients, even those with left ventricular hypertrophy. This may reflect the consequences on the left ventricle of long-term antihypertensive treatment. If complex ventricular arrhythmias are implicated in the excess of sudden deaths in hypertensive patients, this might be an important factor.

QT intervals and QT dispersion as measures of left ventricular hypertrophy in an unselected hypertensive population.

Electrocardiographic (ECG) QT intervals and dispersion correlate with echocardiographic left ventricular mass index (LVMI) in groups of selected essential hypertensives. We tested the strength of this relationship in a large group of unselected hypertensives to assess whether QT measurements may be a simple screening test for LVH in clinical practice. In a cross-sectional study of 386 unselected hypertensive subjects, maximal QT intervals (QTmax), QT dispersion (QTdisp), and ECG voltages (Sokolow-Lyon and Cornell sex-specific voltages) were measured from 12-lead ECG. The LVMI correlated most strongly with Cornell voltage (linear regression r = 0.44, P < .001). The strongest relationship between LVMI and QT parameters was with QTmax, (r = 0.25, P < .001). This relationship weakened using heart rate-corrected QTmax. Correlations between LVMI and QTdisp were weak, whether or not they were corrected for heart rate. Sokolow-Lyon voltages, Cornell voltage and QTmax, but not QTdisp, were independently predictive of LVMI after adjustment for age, sex, race, and the other ECG parameters. Receiver operating characteristic (ROC) curve analyses demonstrated that no QT parameter performed better than simple ECG voltage criteria in the detection of LVH. In conclusion, QTmax, the QT parameter most strongly associated with LVMI, was independently associated with LVMI after adjustment for standard ECG voltage criteria. However, as an isolated measure it was no better than simple ECG voltage criteria as a screening test for LVH in clinical practice.

The effects on cardiac arrhythmias of antihypertensive therapy causing regression of left ventricular hypertrophy.

To examine the effects of antihypertensive therapy causing regression of left ventricular hypertrophy on cardiac arrhythmias, 26 hypertensive subjects were treated with ramipril with felodipine if required, and followed for 6 months after blood pressure control. Compared with baseline, left ventricular mass index (LVMI) was significantly reduced both at blood pressure control and after a further 6 months of treatment (baseline, blood pressure control, 6 months after blood pressure control; LVMI 142 +/- 3.6, 131 +/- 3.4, 123 +/- 3.8* g/m2, *P < .01 compared with baseline). There was a significant relationship between the decrease in systolic blood pressure and the decrease in LVMI after 6 months of blood pressure control compared with baseline (r = 0.41, P = .05). Compared with baseline, the average total number of ventricular ectopics decreased after blood pressure was controlled (88 +/- 59 and 21 +/- 12 respectively); however this reduction was not maintained after 6 months of further treatment, either before (78 +/- 50) or after drug washout (86 +/- 40). Compared with baseline (639 +/- 590) supraventricular ectopic total was not initially reduced after blood pressure control (650 +/- 604), but was reduced after a further 6 months of treatment (294 +/- 261). This reduction was maintained after drug washout (267 +/- 254), although this did not reach statistical significance. Radionuclide scanning at baseline was not a predictor of patients with the highest risk of arrhythmia and there was no correlation between improvement or worsening of a defect with changes in ventricular ectopic total. In conclusion, antihypertensive therapy with ramipril and felodipine, although causing regression of left ventricular hypertrophy did not lead to a sustained reduction in ventricular ectopic total.

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.

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.

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

Left ventricular geometry in presenting untreated hypertension.

In order to investigate the spectrum of geometry in our patient population, 63 untreated hypertensives underwent two-dimensional echocardiography. Left ventricular (LV) mass index and relative wall thickness, a measure of wall thickness in relation to cavity size, were calculated from the M-mode strip. In addition, to assess the sphericity of the left ventricle the ratio of LV minor to major hemiaxis was calculated. The subjects comprised 41 men (17 Caucasian, 22 Afro-Caribbean and two Oriental), and 21 women (five Caucasian, 12 Afro-Caribbean and two Oriental). Concentric hypertrophy was present in 46% of subjects, concentric remodelling in 32% of subjects, eccentric hypertrophy in only 6% of subjects and a normal left ventricular shape in 16% of subjects. The degree of sphericity of the left ventricle was similar among the four groups, suggesting that it does not change in uncomplicated hypertension. In contrast to the previously published combined series from Sassari and New York we had a low proportion of patients with either eccentric hypertrophy or normal left ventricular geometry. This is probably due to the high proportion of Afro-Caribbean subjects in our clinic population who are more likely to have left ventricular hypertrophy.

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

Structural changes in the heart and carotid arteries associated with hypertension in humans.

Hypertension is associated with structural changes in the vascular system and in the heart. This study has examined the relationships between carotid artery intima-media thickness and other risk factors in 52 untreated patients (20 hypertensive). Carotid intima-media thickness was measured bilaterally using a Duplex doppler ultrasonic scanner. In the hypertensive individuals the left ventricle was examined by echo-cardiography and the left ventricular mass index determined. There was a significant association between age and IMT, and both SBP and DBP and IMT. The IMT in the hypertensive group was significantly larger than in the normotensive group and in the hypertensive subjects there was a positive association between left ventricular mass index and IMT. There was no significant difference in calculated media stress between the normotensive and hypertensive groups, probably due to a small increase in carotid intima-media area combined with a small reduction in carotid lumen diameter. Hypertension is associated with a thickening of the intima-media of the carotid artery and an increase in left ventricular mass. Whether these changes in cardiac and arterial structure are in response to similar influences remains to be established.

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.

Left ventricular hypertrophy, blood pressure and ACE genotype in untreated hypertension.

It has been suggested that the deletion polymorphism of the angiotensin-converting enzyme (ACE) genotype may be important in the development of left ventricular hypertrophy (LVH). In order to test this hypothesis we investigated the interaction between blood pressure (BP), LVH and ACE genotype in 86 previously untreated hypertensive patients. Each underwent two-dimensional and Doppler echocardiography and ACE genotyping. There were no significant differences in BP, the parameters of left ventricular structure (including left ventricular mass index) or diastolic function between the three genotype groups. Additionally, there were no significant differences in the relationship between systolic BP and left ventricular mass index among the three genotype groups (II genotype, r = 0.46, P = 0.02; ID genotype, r = 0.42, P = 0.01; DD genotype, r = 0.34, P = 0.10; F = 0.38). In contrast to some previous studies, we have found in this group of previously untreated hypertensive subjects no evidence to suggest that the deletion polymorphism of the ACE genotype is important in the development of LVH.

Left ventricular diastolic function in hypertension: a 4 year follow-up study.

In order to assess the long term effects of antihypertensive treatment on left ventricular diastolic function, 26 hypertensive patients were followed up for a mean of 4.25 years with two-dimensional and Doppler echocardiography. A significant reduction in left ventricular mass index was first apparent after 9 months of therapy (mean (S.D.) 124 (22) vs. 114 (18) g/m2, P < 0.01), and this was maintained over the 4.25 year period (124 (22) vs. 117 (17) g/m2, p < 0.05). At 9 months there was no change in either isovolumic relaxation time (108 (26) vs. 108 (17) ms, P = N.S.) or left ventricular filling as assessed by peak flow velocity E/A ratio (0.94 (0.22) vs. 0.95 (0.27), P = N.S.). However, after 4.25 years there was a significant improvement in IVRT (108 (26) vs. 83 (11) ms, P < 0.01) with a trend towards an improved peak flow velocity E/A ratio, although this did not reach statistical significance (0.95 (0.27) vs. 1.02 (0.26), P = N.S.). Of the 14 patients who had an abnormal isovolumic relaxation time at baseline, 12 normalised and 2 improved. These findings suggest that left ventricular diastolic dysfunction in hypertension may be reversed by prolonged antihypertensive treatment.