Haemodynamic effects of changes in atrioventricular and interventricular delay in cardiac resynchronisation therapy show a consistent pattern: analysis of shape, magnitude and relative importance of atrioventricular and interventricular delay.

OBJECTIVE: To assess the haemodynamic effect of simultaneously adjusting atrioventricular (AV) and interventricular (VV) delays. METHOD: 35 different combinations of AV and VV delay were tested by using digital photoplethysmography (Finometer) with repeated alternations to measure relative change in systolic blood pressure (SBP(rel)) in 15 patients with cardiac resynchronisation devices for heart failure. RESULTS: Changing AV delay had a larger effect than changing VV delay (range of SBP(rel) 21 v 4.2 mm Hg, p < 0.001). Each had a curvilinear effect. The curve of response to AV delay fitted extremely closely to a parabola (average R2 = 0.99, average residual variance 0.8 mm Hg2). The response to VV delay was significantly less curved (quadratic coefficient 67 v 1194 mm Hg/s2, p = 0.003) and therefore, although the residual variance was equally small (0.8 mm Hg2), the R2 value was 0.7. Reproducibility at two months was good, with the SD of the difference between two measurements of SBP(rel) being 2.5 mm Hg for AV delay (2% of mean systolic blood pressure) and 1.5 mm Hg for VV delay (1% of mean systolic blood pressure). CONCLUSIONS: Changing AV and VV delays results in a curvilinear acute blood pressure response. This shape fits very closely to a parabola, which may be valuable information in developing a streamlined clinical protocol. VV delay adjustment provides an additional, albeit smaller, haemodynamic benefit to AV optimisation.

The effect of adjusting for baseline risk factors and post revascularisation coronary disease on comparisons between coronary angioplasty and bypass surgery.

BACKGROUND: In CABRI at 1 year PTCA was associated with greater repeat revascularisation and angina (but not myocardial infarction or death). We determined whether adjusting for baseline risk factors and post revascularisation coronary disease offsets this disadvantage of PTCA. METHODS: In the CABRI population the crude association of revascularisation mode (i.e. PTCA or CABG) with four clinical outcome (i.e. mortality, myocardial infarction, repeat revascularisation and angina) was adjusted for the baseline risk factors using a logistic regression model for each clinical outcome. A number of measures of angiographic coronary disease were used to assess post revascularisation coronary disease. One at a time, each of these measures was added to each of the four outcome models, to adjust for post revascularisation coronary disease. RESULTS: Comparing adjusted and crude unadjusted association of PTCA with repeat revascularisation there was an increase from 12.8 (P<0.0005) (crude relative risk) to 16.7 (P<0.0005) (adjusted odds ratio), with angina, from 1.89 (P=0.001) to 1.98 (P<0.0019), and with mortality from 1.84 (P=0.092) to 2.15 (P=0.060). PTCA was not significantly associated with myocardial infarction, either crudely or after adjustment. CONCLUSION: Adjusting for baseline risk factors and post revascularisation coronary disease tended to strengthen rather than weaken associations between PTCA and 1 year mortality, repeat revascularisation and angina at 1 year.

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.

Relation between coronary artery disease, baseline clinical variables, revascularization mode, and mortality. CABRI Participants. Coronary Angioplasty vs. Bypass Revascularisation Investigation.

The Coronary Angioplasty vs. Bypass Revascularisation Investigation (CABRI) trial comparing percutaneous transluminal coronary angioplasty (PTCA) with coronary artery bypass grafting did not show a difference in mortality with either procedure. Nonrandomized studies suggest that coronary artery disease (CAD) severity and distribution influences outcome. In the present study we explored the effect of prerevascularization CAD on 1-year mortality in the CABRI population, while adjusting for other baseline variables. Of the 1,054 patients recruited, there were sufficient angiographic results to derive the CAD scores in 974 (92.4%). Of these 974, there were 32 deaths. A number of CAD scores, both weighted for proximal disease (Duke and Leaman) and nonweighted, were used. These scores were then cross-tabulated against mortality. Demographic and clinical variables were also cross-tabulated against mortality and used to derive an initial logistic regression model to predict mortality. The effect of adding each of the CAD scores to this initial model was then assessed. After inclusion of the CAD scores, the best model was: (1) presence of peripheral vascular disease (odds ratio [OR] 3.89, p = 0.0025), (2) previous cerebrovascular accident (OR 2.86, p = 0.043), (3) older age (OR 1.05, p = 0.039), (4) a higher Duke score (OR 2.84, p = 0.0061), and (5) having undergone PTCA (OR 2.12, p = 0.047). In the CABRI population, adjustment for baseline variables, including prerevascularization CAD, revealed significantly higher mortality in those who underwent PTCA than in those who underwent coronary artery bypass grafting.

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

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.

Effect of alpha1-adrenoceptor blockade on coronary vasodilator reserve in cardiac syndrome X.

We sought to test the response of the coronary microcirculation to alpha-adrenoceptor blockade in patients with syndrome X (angina, ischemia-like stress electrocardiogram, and a normal coronary arteriogram). The response of the microcirculation was assessed by quantification of coronary vasodilator reserve (the ratio of hyperemic to resting myocardial blood flow). We investigated 28 patients with syndrome X [18 women, age 54.4 (7.6) years]. Myocardial blood flow was measured at rest and after dipyridamole by using positron emission tomography with H(2)15O. The measurements were made before and after treatment for 10 days with doxazosin (1 mg o.d. for 3 days, followed by 2 mg o.d. for 7 days) or a matched placebo, similarly administered. Patients were randomized to alpha1-blockade or to placebo in double-blind fashion. No significant differences were demonstrable between syndrome X patients treated with doxazosin and those receiving placebo, with respect to resting myocardial blood flow, myocardial blood flow after dipyridamole, or coronary vasodilator reserve (the ratio of the latter two). In addition, no relations were demonstrable among myocardial blood flow, coronary vasodilator reserve, development of chest pain after dipyridamole, or development of ischemia-like ECG changes. Doxazosin had no effect on the perception of chest pain after dipyridamole. No differences were found between the effects of alpha1-blockade with doxazosin or those of placebo with respect to myocardial blood flow in syndrome X. The values obtained for myocardial blood flow and coronary vasodilator reserve for the patients were within the normal range. The data do not support the case for alpha1-mediated vasoconstriction having an etiologic role in the chest pain of syndrome X.

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.

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.

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.

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.

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.

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.

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.

Minimally invasive coronary revascularization through parasternal incisions without cardiopulmonary bypass.

BACKGROUND: We report the results of minimally invasive coronary revascularization without cardiopulmonary bypass through miniparasternal incisions. METHODS: This procedure was performed in 40 patients with disease in the left anterior descending, first diagonal, and right coronary arteries. After a 5- to 7-cm left vertical parasternal incision and removal of two costal cartilages, the left internal mammary artery was harvested up to the 2nd rib. The left anterior descending artery was occluded by means of two polydioxanone monofilament sutures. The anastomosis was performed with one 7-0 Prolene suture while the heart was beating. In 4 cases the left internal mammary artery was used as a sequential graft to the left anterior descending artery and the first diagonal artery. In 14 cases the right coronary artery was grafted with the right internal mammary artery through a right parasternal incision. Postoperatively, 95% of the patients underwent angiographic assessment of the anastomoses. RESULTS: We performed 52 anastomoses (34 to the left anterior descending artery, 4 to the first diagonal artery, and 14 to the right coronary artery). The mortality was 0% and the morbidity included postoperative bleeding (5%), acute renal failure (2.5%), atrial fibrillation (2.5%), and wound infection (5%). No patient had ventricular arrhythmias or circulatory problems during or after the operation. Two patients (5%) with right internal mammary artery-to-right coronary artery grafting had graft failure that required a redo operation. CONCLUSIONS: Small vertical parasternal incisions may be an alternative approach for single and multiple coronary revascularization, with a low incidence of intraoperative cardiac complications. The application of this approach to the right coronary artery, however, carries additional technical difficulties, and careful patient selection may be required to achieve optimal results.

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.