Diastolic relaxation and left ventricular blood filling in patients with hypertension

Disorders of left-ventricular diastolic relaxation and blood filling in patients with first- and second-stage essential hypertension are shown, by means of echo-, radio- and apexcardiography, to be due to the effects of arterial blood pressure, hemodynamic changes, heart rate and the magnitude of left-ventricular hypertrophy. Antihypertensive treatment, affecting major parameters of disease, brings about the recovery of the heart's diastolic function.     

Improved left ventricular filling accompanies reduced left ventricular mass during therapy of essential hypertension

Abnormal left ventricular diastolic performance, an early manifestation of hypertension in the heart, may precede the development of left ventricular hypertrophy. To assess effects of antihypertensive therapy on the heart, left ventricular mass (determined by echocardiography) and rapid left ventricular filling rate (determined by radionuclide ventriculography) were compared before and after 6 months of treatment of 16 patients. Nitrendipine (a dihydropyridine calcium channel blocker) was given alone or in combination with either propranolol or hydrochlorothiazide, or both, and significantly reduced blood pressure (156/103 +/- 12/7 to 137/89 +/- 10/6 mm Hg). In 6 of the 16 patients, left ventricular mass decreased by more than 10% (270 +/- 95 to 193 +/- 47 g, p less than 0.01); in the same patients, left ventricular filling rate increased (2.03 +/- 0.35 to 2.30 +/- 0.45 end-diastolic counts/s [EDC/s], p less than 0.01). In the one patient whose left ventricular mass increased (137 to 195 g), left ventricular filling rate decreased from 2.01 to 1.78 EDC/s. In the remaining nine patients who had no change in left ventricular mass, there was no significant changes in left ventricular filling. The changes in ventricular mass and filling could not be related to the extent of change in blood pressure or heart rate. These data suggest that regression of left ventricular mass during antihypertensive therapy with nitrendipine is accompanied by improved diastolic function.     

Diastolic properties of hypertrophied hearts in essential hypertension: classification by left ventricular wall stress

Hypertensive cardiac hypertrophy of 20 patients was classified as inappropriate hypertrophy (HH-I) and appropriate hypertrophy (HH-II) according to their end-systolic wall stress, as measured by echocardiography. The differences in systolic and diastolic performances among the HH-I and HH-II subjects and 10 normal controls (NC) before and during isoproterenol infusion were investigated. Eight patients had subnormal end-systolic wall stress (inappropriate hypertrophy) and 12, normal end-systolic wall stress (appropriate hypertrophy). Before isoproterenol infusion, normalized peak rate of a change in left ventricular diameter during systole was significantly greater in HH-I (3.5 +/- 0.8/s) than in NC (2.3 +/- 0.5/s) and HH-II (2.6 +/- 0.6/s) (p less than 0.01 and p less than 0.005), but there was no significant difference between HH-II and NC. There was no significant difference in normalized peak rate of a change of left ventricular diameter during the rapid filling phase among the three groups (4.5 +/- 1.2/s in HH-I, 4.0 +/- 1.6/s in HH-II, and 4.2 +/- 0.8/s in NC). During isoproterenol infusion, normalized peak rate of a change of left ventricular diameter during systole was significantly greater in HH-I (7.0 +/- 1.9/s) than in HH-II (4.8 +/- 1.7/s) and NC (4.8 +/- 0.8/s) (p less than 0.05 and p less than 0.01, respectively), but there was no significant difference between HH-II and NC. Normalized peak rate of a change of left ventricular diameter during rapid filling was significantly less in HH-II (4.8 +/- 1.7/s) than in HH-I (7.3 +/- 1.3/s) and NC (6.5 +/- 0.8/s) (p less than 0.005 and p less than 0.005, respectively), but there was no significant difference between HH-I and NC. These results suggest that hypertensive patients with inappropriate hypertrophy have relatively diminished diastolic velocity (supernormal systolic velocity and normal diastolic velocity) before and during isoproterenol infusion, and that hypertensive patients with appropriate hypertrophy have absolutely diminished diastolic velocity during isoproterenol infusion, in spite of normal diastolic velocity before the infusion.     

Suppression of left ventricular early diastolic filling by long axis asynchrony.

OBJECTIVE--To assess how early diastolic transmitral flow is suppressed in a group of patients in whom effective ventricular filling occurred exclusively with atrial systole. DESIGN--Prospective examination of the left ventricular transverse and longitudinal axes and transmitral Doppler flow. SETTING--A tertiary referral centre for cardiac diseases. SUBJECTS--20 patients (mean (SD) age 65 (10) years) with isolated transmitral late diastolic flow were studied. None had sinus tachycardia, prolonged PR interval or a summation flow pattern. 21 normal individuals of similar age served as controls. RESULTS--The left ventricle was usually dilated, end diastolic diameter (6.6 (1.0) v 4.9 (0.5) cm, P < 0.001) and end systolic diameter (5.4 (1.1) v 3.3 (0.5) cm, P < 0.001) were both increased, and fractional shortening of the minor axis reduced (16 (7)% v 30 (10)%, P < 0.001) in patients in whom left ventricular early diastolic filling was absent compared with those of normal controls. Mitral valve opening was late after aortic valve closure (A2) (115 (30) v 60 (10) ms, P < 0.001). The minor axis increased during this period (30 (20)% v 8.6 (2.5)%, P < 0.001). Onset of detectable transmitral flow was further delayed after cusp separation (85 (25) v 25 (10) ms, P < 0.001). Left ventricular long axis function was very abnormal. Onset of shortening was delayed with respect to the q wave at the left and septal sites (150 (40) v 90 (20) ms and 145 (30) v 80 (10) ms respectively, P < 0.001) and major shortening occurred after, rather than before, A2 (25 (12) v -10 (2.5)% and 50 (30) v -6.6 (0.3)% total excursion, P < 0.001). Although the long axis lengthened a little at the start of early diastole, its dominant component occurred in late diastole to coincide with atrial systole. The relative A wave was thus greatly increased at both sites (67 (17) v 29 (6)% and 77 (13) v 33 (8)%, P < 0.001). CONCLUSION--Prolonged left ventricular long axis shortening and delayed onset of lengthening effectively suppress early diastolic transmitral flow even though the minor axis increases and mitral cusps separate apparently normally. This grossly asynchronous left ventricular relaxation may interfere with filling by dissipating normal ventricular restoring forces.     

Influence of left ventricular asynchrony on filling in coronary artery disease

To evaluate whether the extent of left ventricular (LV) asynchrony plays a role in the impairment of LV rapid filling in patients with coronary artery disease (CAD), 48 patients underwent both radionuclide angiography and cardiac catheterization. Patients were divided into group I (n = 33), with normal LV kinesis or only mild hypokinesia, and group II (n = 15), with LV dyskinesia or akinesia. Radionuclide ejection fraction was higher in group I than in group II (62 +/- 12 vs 44 +/- 20%; p less than 0.001). Peak filling rate was significantly lower in group II (1.9 +/- 0.8 vs 2.6 +/- 0.9 end-diastolic counts/s; p less than 0.01). Time to end-systole coefficient of variation, an index of the extent of LV asynchrony, was significantly higher in group II than in group I (43 +/- 10 vs 35 +/- 6; p less than 0.0002). In group I, a highly significant inverse relation was found between this index of asynchrony and peak filling rate (r = 0.71; p less than 0.0001). This correlation was found even when time to end-systole coefficient of variation was normalized to the RR interval (r = 0.49; p less than 0.01) and when peak filling rate was expressed in stroke counts (r = 0.57; p less than 0.001). The correlation between peak filling rate and index of asynchrony was maintained up to an end-systole coefficient of variation value of approximately 35. In group II patients (most with an asynchrony value greater than or equal to 35) no relation was found between time to end-systole coefficient of variation and peak filling rate.     

Determinants of left ventricular filling in hypertension

The relationship of left ventricular (LV) filling to the clinical and echocardiographic characteristics of 51 patients with untreated hypertension (borderline hypertension n = 17, essential hypertension n = 34) was investigated using two-dimensional echocardiography and Doppler ultrasound. Twenty-five patients had evidence of abnormal LV filling. Linear regression analysis revealed weak but significant correlations of LV filling with age (r = -0.53; P less than 0.0001), systolic blood pressure (r = -0.38; P less than 0.006), LV septal wall thickness (r = -0.44; P less than 0.0001) and LV mass index (r = -0.33; P less than 0.02). There was no association between LV filling and sex, race, heart rate or LV posterior wall thickness or cavity dimension. After stepwise regression analysis, age was found to be the only independent variable associated with LV filling, indicating that the other variables were dependent on age. This study suggests that a) abnormal LV filling is a frequent observation in hypertension b) LV filling is more dependent on age than blood pressure or LV size and c) other pathophysiological factors, so far undetermined, must contribute to the development of these abnormalities.     

Regional left ventricular asynchrony and impaired global left ventricular filling in hypertrophic cardiomyopathy: effect of verapamil

Left ventricular relaxation and filling are impaired in many patients with hypertrophic cardiomyopathy. To investigate the influence of regional heterogeneity on these global abnormalities, 48 patients with hypertrophic cardiomyopathy and sinus rhythm were studied by radionuclide angiography before and after 1 to 2 weeks of verapamil therapy (320 to 640 mg/day, median 480). Left ventricular regional function was assessed by subdividing the ventricular region of interest into 20 sectors and into four quadrants from which regional time-activity curves were derived. Diastolic asynchrony was measured as the regional variation in timing between minimal volume and peak filling rate, and heterogeneity in the magnitude of rapid diastolic filling was measured as the regional variation in percent contribution of atrial systole to end-diastolic volume. Compared with 28 normal subjects, the patients with hypertrophic cardiomyopathy had greater regional variation in both timing (35 +/- 24 versus 12 +/- 6 ms, p less than 0.001) and magnitude (10 +/- 6 versus 7 +/- 4%, p less than 0.02) of rapid filling. Verapamil reduced the regional variation in timing (to 21 +/- 16 ms, p less than 0.001) and magnitude (to 7 +/- 3%, p less than 0.001) of rapid filling. These regional changes, indicating more uniform regional diastolic performance after verapamil, were associated with improved global diastolic filling: global rapid filling increased in both rate and magnitude and time to peak filling rate decreased. These findings indicate that the beneficial effect of verapamil on left ventricular diastolic function in hypertrophic cardiomyopathy may be mediated by reduction in regional asynchrony.     

Impact of dietary sodium intake on left ventricular diastolic filling in early essential hypertension

Aims Dietary sodium intake modulates left ventricular hypertrophyin established essential hypertension independent of blood pressurelevel. We conducted this study to elucidate the relationshipbetween sodium intake and left ventricular structural or functionalchanges in early essential hypertension. Methods Forty-four young male patients (age 25·9±2·6years) with mild essential hypertension that had never beentreated and 45 normotensive male control subjects of similarage were examined. Dietary sodium intake was measured from 24hurinary sodium excretion, blood pressure from 24h ambulatorymonitoring (SpaceLabs 90207), left ventricular structure from2-D guided M-mode echocardiography, and diastolic filling ofthe left ventricle (as the main compound of diastolic functionin a young population) by pulse-wave Doppler sonography. Results In hypertensive patients, daily sodium excretion correlatedwith the ratio of late (A) to early (E) maximum velocity (VmaxA/E; r=+0·27,P=0·07), velocity time integrals(A/E; r=+0·54,P<0·001) as well as atrial contribution,as a percent of left ventricular filling (VH ATCO; r=+0·52,P<0·001)independent of heart rate, whereas the opposite correlationswere observed in normotensives (allP<0·001). Stepwisemultiple regression analysis confirmed these results. Sodiumexcretion emerged as the strongest independent determinant ofimpaired diastolic filling in hypertensive patients (velocitytime integrals A/E: R²=0·49, ß=+0·57,P=0·0001;VH ATCO: R²=0·48, ß=+0·56,P<0·0001;Vmax A/E: ns). In normotensive subjects, sodium excretion wasa similar strong, but inverse deter-minant of diastolic filling(velocity time integrals A/E: R²=0·40, ß=–0·43,P=0·0028).Heart rate was a strong determinant of diastolic filling inhypertensive patients (ß=+0·55,P=0·0002)and in normotensive subjects (ß=+0·34,P=0·011).Left ventricular mass and end-diastolic volume index were notrelated to diastolic filling in either group. Conclusion In early essential hypertension, sodium excretion is correlatedwith impaired left ventricular diastolic filling independentof left ventricular mass. The renin-angiotensin-aldosteronesystem might be a mediator of the observed correlation.     

Left ventricular hypertrophy and impaired diastolic filling in essential hypertension. Diastolic mechanisms for systolic dysfunction during exercise

Left ventricular ejection fraction is normal at rest but may respond abnormally to exercise in many patients with essential hypertension. To assess the determinants of the abnormal ejection fraction response to exercise, we performed radionuclide angiography at rest and during exercise in 41 hypertensive patients without coronary artery disease. In 22 patients (group 1), the ejection fraction increased more than 5% during exercise; in the other 19 patients (group 2), the ejection fraction either increased by less than 5% or decreased with exercise. Left ventricular diastolic filling was impaired at rest in patients in group 2 compared with group 1, with reduced peak filling rate (2.5 +/- 0.4 vs. 3.1 +/- 0.7 end-diastolic volume/sec; p less than 0.01) and prolonged time to peak filling rate (175 +/- 28 vs. 153 +/- 22 msec; p less than 0.01). Impaired diastolic filling in group 2 was associated with less augmentation in end-diastolic volume during exercise compared with group 1 (p less than 0.01). These observations were not dependent on the threshold value that was arbitrarily chosen to define an abnormal ejection fraction response, as there were significant correlations for the entire group between the magnitude of change in ejection fraction with exercise and both the resting peak filling rate (r = 0.46) and the change in end-diastolic volume with exercise (r = 0.62).(ABSTRACT TRUNCATED AT 250 WORDS)     

Diastolic filling in acute left ventricular dysfunction: role of the pericardium

Patients with congestive heart failure and elevated left ventricular filling pressures demonstrate an abnormal pattern of diastolic filling that is characterized by a redistribution of diastolic filling to early diastole with reduced reliance on late diastolic filling. The diastolic filling pattern superficially resembles that which is seen with constrictive pericarditis. To examine potential mechanisms for these clinical findings, a model of ischemic left ventricular dysfunction was produced in seven dogs by repeated coronary microsphere embolization, producing a dilated left ventricle with reduced systolic function. Measurements of left ventricular systolic and end-diastolic pressures, rate of rise of left ventricular pressure (dP/dt) and echocardiographic end-diastolic and end-systolic areas were obtained at baseline, during intermediate embolization (moderate left ventricular systolic dysfunction, dilation and mild increases in left ventricular end-diastolic pressure), postembolization (further embolization resulting in severe left ventricular systolic dysfunction, dilation and marked increases in left ventricular end-diastolic pressure), after thoracotomy and after pericardiectomy. The filling fraction at 1/3 and 1/2 of diastole and the time constant of left ventricular pressure decline were also determined. Repetitive coronary microembolization caused progressive left ventricular dilation and decreasing systolic function, which did not change after opening the chest or pericardium. The filling fraction at 1/3 and 1/2 of diastole declined with intermediate embolization (12.0 +/- 5.6% and 23.1 +/- 10.8%, respectively) as compared with baseline values (29.0 +/- 11.9%, 42.9 +/- 15.6%, p less than 0.05). After embolization, there was an increase in the 1/3 and the 1/2 filling fraction (47.5 +/- 8.9%, 72.0 +/- 6.0%, respectively, p less than 0.01) as compared with baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Diastolic regional wall motion asynchrony in patients with hypertension

Left ventricular regional wall motion was analyzed from angiographic ventriculograms in 51 subjects, 18 of these served as controls, 10 were hypertensive with coronary artery disease, and 23 had a history of hypertension without coronary artery disease. All normal subjects showed normal synchronous wall motion throughout the cardiac cycle. In 10 patients with coronary artery disease and hypertension at the time of catheterization, the major determinant of regional abnormality was coronary artery lesion (sensitivity=83%, specificity=95%). Patients who had a history of hypertension and no ischemic disease, were further subdivided into three groups, 4 who were normotensive, 4 with borderline pressures and 15 hypertensive at the time of cardiac catheterization. All normotensive, 3 of the borderline hypertensive, as well as one hypertensive (without coronary artery disease) patients showed normal wall motion. In one patient with borderline pressure and 14 of 15 hypertensive patients diastolic regional asynchrony was detected. Apical region was most commonly affected in these patients. This suggests the importance of treating hypertension in patients and the possible reversibility of abnormal wall motion with treatment.     

Normal aging, hypertension and left ventricular filling

Because of discrepancy in interpretation of early diastolic filling indices in normal subjects and hypertensive, we studied the correlations between age and radionuclide angiographic peak filling rate (PFR), doppler echocardiographic early E and late A waves, left ventricular mass (LVM), blood pressure (BP) and ejection fraction (EF) in cautiously screened 30 untreated hypertensive and 30 age paired normal subjects (mean of age 52 +/- 17 ranging from 34 to 78 years). No patient had gross obesity nor coronary artery disease. Univariate analysis revealed strong correlations between LV filling and age in normal (r = -0.82 p less than 0.0001) and hypertensive (r = -0.61 p less than 0.001), with a very significant difference in y intercepts (t = 0.61 p = 10(-6)). LVM correlated poorly with age (r = 0.35 p less than 0.05) but with none of the LV filling indexes. BP correlated with PFR (r = 0.33 p less than 0.05) and A wave (r = 0.44 p less than 0.02) in hypertensive only. After multivariate analysis, significant dependencies of PFR, age, LV mass were more accurate if BP was in a higher range. The variability of the values of LV filling indexes was wider in hypertensive than in normotensive. Normotensive aging and hypertension have similar effects on the cardiovascular system. In the most aged people even without apparent cardiac disease, it is not possible to identify the specific effects of hypertension on diastolic function.     

Determinants of abnormal left ventricular filling in early hypertension

Thirty-seven untreated subjects with borderline or mild hypertension were studied to establish the prevalence and clinical characteristics associated with abnormal left ventricular filling in this disorder. Subjects were referred to this study because of casual office blood pressure measurements of greater than or equal to 140/90 mm Hg; all were less than 50 years old, had no other cardiovascular or systemic disease and had not received antihypertensive medication for at least 1 year. To precisely determine blood pressure, measurements were made over 30 min with the patient in the supine position and during awake hours with ambulatory monitoring. Left ventricular mass was determined echocardiographically, and Doppler echocardiography was used to assess left ventricular filling. No subject had increased left ventricular mass, but 8 (22%) of the 37 had abnormal left ventricular filling. All eight subjects with abnormal left ventricular filling had an ambulatory systolic blood pressure greater than 130 mm Hg and a supine systolic blood pressure greater than 122 mm Hg. Abnormal filling was not related to left ventricular mass or heart rate. In multivariate analysis, the degree of abnormal filling could best be predicted from a combination of age and supine systolic blood pressure (r = 0.69; p less than 0.001). This study suggests that in untreated early essential hypertension, abnormal left ventricular filling is present in greater than 20% of subjects, precedes detectable left ventricular hypertrophy and is related to age and prevailing level of blood pressure.     

Different patterns of left ventricular filling in arterial hypertension

To determine whether left ventricular (LV) filling dynamics may be influenced by the type of LV morphological adaptation to arterial hypertension, pulsed Doppler mitral flow velocity recordings were performed in 30 hypertensive patients and in 18 normotensive subjects matched for age, body surface and heart rate. Peak early (E) and late (A) mitral flow velocity, A/E ratio (A/E), time to peak E (TP), acceleration (AHT) and deceleration half-time (DHT) of early mitral flow and isovolumic relaxation time (IRT) were measured. Compared with the control group, hypertensive patients showed prolonged IRT and DHT, increased A and A/E, whereas TP, AHT and E were unchanged. Hypertensive patients were classified into two subgroups on the basis of h/r ratio (h/r). Subgroup 1: 16 patients with normal h/r, less than 0.42, (five patients with increased LV mass index, greater than 129.2 g m-2, and 11 patients with normal LV mass index, less than 129.2 g m-2). Subgroup 2: 14 patients with increased h/r, greater than 0.42, (nine patients with increased LV mass index, greater than 129.2 g m-2 and five patients with normal LV mass index, less than 129.2 g m-2). In Subgroup 1 the cardiac output (CO) was increased and the total peripheral resistance (TPR) was unchanged in comparison with the control group. In Subgroup 2 the opposite haemodynamic profile was detected: normal CO and increased TPR.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular filling and stress response pattern in essential hypertension

PURPOSE: To evaluate whether impaired left ventricular filling determines the hemodynamic responses to isometric and orthostatic stress in a population with mild essential hypertension. PATIENTS AND METHODS: The study population consisted of 32 patients with essential hypertension who were subdivided into those with preserved left ventricular filling (15 patients) and those with impaired left ventricular filling (17 patients). Echocardiograms were obtained before hemodynamic assessment was performed. Isometric stress and head-up tilt tests were done with a recovery period of at least 10 minutes between each to allow for blood pressure and heart rate to return to baseline. Hemodynamic reassessment was performed during the last minute of each test and at the end of the recovery period. Plasma epinephrine, norepinephrine, and dopamine levels were determined by radioenzymatic method. RESULTS: Isometric stress increased mean arterial pressure by 30% (p less than 0.0001) by an increase in cardiac output (p less than 0.0001) and total peripheral resistance (p less than 0.0001) associated with an increase in plasma catecholamine levels (p less than 0.0001). Patients with preserved left ventricular filling had an increase in arterial pressure predominantly through an elevation in cardiac output (17%, p less than 0.0001) associated with a small increase in plasma norepinephrine levels (p less than 0.05) and in peripheral resistance (11%, p less than 0.05). In contrast, patients with impaired left ventricular filling had an increase in arterial pressure mainly through an increase in peripheral resistance (25%, p less than 0.0001) that was associated with a 45% elevation in plasma norepinephrine levels (p less than 0.0001). Orthostatic stress (passive head-up tilt) caused an exaggerated decrease in stroke volume (p less than 0.01) and cardiac output (p less than 0.01) in patients with impaired left ventricular filling when compared with those with preserved diastolic function. CONCLUSION: Impaired left ventricular filling blunts the response of the heart to isometric and orthostatic stress. As a consequence, hypertensive patients with impaired ventricular filling respond to these stressors with enhanced sympathetic stimulation and exaggerated vasoconstriction.     

Correction of left ventricular asynchrony by coronary artery surgery

To investigate the effect of coronary artery bypass grafting on the timing of regional left ventricular wall motion, contrast left ventriculograms from 27 patients were digitised frame by frame before and after operation. End diastolic and end systolic volumes, ejection fraction, and peak ejection and filling rates showed no significant change. The commonest preoperative abnormality was delayed onset of inward wall motion during ejection, which was present in 14 patients over 10% (range 5-40%) of the cavity outline, leading to a pattern of "diagonal contours". After operation this pattern had resolved completely in 12 patients and partially in two. Minor abnormalities appeared postoperatively in five but overall the mean (1SD) area affected was reduced by 5 (8)%. The time span between the onset of inward motion in different regions of the cavity also fell significantly after surgery from 190 (50) to 130 (50) ms. Regional hypokinesis (6 cases) and abnormal wall motion during isovolumic contraction (4 cases) or isovolumic relaxation (5 cases) were not consistently affected. Thus successful coronary artery surgery is without consistent effect on overall left ventricular function, overall hypokinesis, or abnormal wall motion during the isovolumic periods. It does, however, strikingly reduce the asynchrony of wall motion during ejection, suggesting that before operation this abnormality may directly reflect impaired coronary blood flow. The results emphasise the potential value of analysing regional wall motion to elucidate functional abnormalities associated with coronary artery disease.     

高血压病对左室功能的影响

目的探讨高血压病患者心脏左室功能的改变. 方法应用超声心动图及组织多普勒显像(DTI)检测74例高血压病患者及94例正常对照者左室收缩及舒张功能. 结果高血压病组左室质量指数、跨二尖瓣血流频谱速度A及E/A比值和DTI频谱速度s、a及e/a比值较正常组有显著差异(P＜0.05),但左室射血分数(LVEF)、跨二尖瓣血流频谱速度E和DTI频谱速度e在高血压病组及正常组间无显著差异(P＞0.05);DTI的收缩期峰速度与LVEF和舒张期峰速度比值e/a与E/A在两组间均呈显著相关(P＜0.05). 结论高血压病患者收缩期峰速度s及舒张晚期峰速度a增加,提示左室收缩功能增强,左室僵硬度增加,左房辅助泵功能增强;DTI能早期、敏感地发现高血压病患者收缩及舒张功能的改变.     

Ventricular arrhythmias and left ventricular hypertrophy in essential hypertension

BACKGROUND: Patients with essential hypertension and/or left ventricular hypertrophy and ventricular arrhythmias suffer from an increased mortality rate. In all previous studies on hypertension, the criterion for inclusion was diastolic blood pressure > 95 mmHg. This is a low selective threshold. Our study attempted to evaluate the incidence of ventricular arrhythmia in hypertensive patients not receiving pharmacological treatment and diagnosed by 24-h ambulatory blood pressure monitoring (ABPM), therefore using a more selective criterion than WHO guidelines. METHODS: Hundred-twenty-height consecutive patients with hypertension diagnosed on the basis of WHO guidelines were screened for 24-h ambulatory blood pressure measurement. Eighty-five (66.4%) presented a 24-h mean blood pressure > 135/85 mmHg. All 85 patients were screened for M-mode, B-mode echocardiography, PW Doppler and 24-h ECG Holter recordings. RESULTS: Sixty patients (70.6%) were affected by left ventricular hypertrophy and 25 were free (29.4%). Thirty-six patients (42.4%) had left ventricular diastolic dysfunction, 49 were free (57.6%). According to Lown and Wolf's classification of ventricular arrhythmia, 20 patients (23.5%) presented Grade I arrhythmia, 5 (5.9%) presented Grade II, 4 (4.7%) Grade III, 9 (10.6%) Grade IVA, 20 (23.5%) Grade IVB, 12 (14.1%) Grade V and 15 patients (17.6%) were free from premature ventricular complexes, namely Grade 0 arrhythmia. Left ventricular hypertrophy was found to correlate significantly with the arrhythmia score, r = 0.552 for p < 0.0001. Moreover, left ventricular diastolic dysfunction correlated significantly with the arrhythmia score, r = 0.495 for p < 0.0001. There was also a good correlation between left ventricular hypertrophy and left ventricular diastolic dysfunction, r = 0.616 for p < 0.0001. Among patients affected by left ventricular diastolic dysfunction and left ventricular hypertrophy, the correlation with the arrhythmia score was even closer, r = 0.586 for p < 0.0007. CONCLUSIONS: We conclude that by using a more selective criterion for the diagnosis of hypertension, we can identify patients with a highly significant statistical correlation between left ventricular hypertrophy and ventricular arrhythmia score, and also between diastolic dysfunction and the ventricular arrhythmia score, due to a more severe stage of disease. It is useful to detect those patients affected by ventricular arrhythmias for the primary prevention of major cardiovascular events.