Left ventricular mass and hypertrophy assessment by means of the QRS complex voltage-independent measurements

ECG QRS-complex voltage-based criteria are relatively insensitive for detection of increased left ventricular mass (LVM). We developed and evaluate a new ECG index for LV hypertrophy (LVH) detection regardless of the QRS voltage. METHODS: Study population consisted of 106 patients (73 m, 33 f, aged 60 +/- 10 years) with established coronary artery disease (CAD). All patients had LVM assessed echocardiographically and indexed to BSA (LVMI(ECHO)). LVH was diagnosed if LVMI(ECHO) >117 g/m2 in men and >104 g/m2 in women. LV geometry was also determined. Analysed ECG variables, obtained from 12 leads recorded simultaneously, were: the QRS complex duration (QRSd, ms), the average 12-lead time to maximal deflection (TMD, ms), the average 12-lead QRS complex voltage (12QRSV, mV), the average product of 12 lead QRS voltage and duration (12QRSVd, mV ms), Sokolow-Lyon voltage and V-d product (SLV, SLVd), Cornell voltage and V-d product (CV, CVd). A newly developed index, LVM(ECG), was calculated, as LVM(ECG) = [(2 x TMD+QRSd/pi)3-(QRSd/pi)3]*0.0001 (ms3), and indexed to BSA (LVMI(ECG), ms3/m2). RESULTS: Means of the QRS voltage-related parameters were similar in patients with LVH and normal LVM. Greater differences existed between both groups when the QRS voltage-duration products were compared. LVMI(ECG) was most powerful in distinguishing between groups (130 +/- 33 LVH vs 91 +/- 21 normal LVM, p < 0.001). LVMI(ECG) correlated with LVMI(ECHO) better (r = 0.77, p < 0.001) than other indices (r coefficients between 0.24 for SLV and 0.49 for CVd). None of the examined indices allowed for distinction between eccentric and concentric LVH. The new index showed better statistical performance (area under ROC = 0.861) compared to the other indices (AUC range 0.545-0.697, p<0.001 vs LVMI(ECG)). At the specificity level of 92%, the value of LVMI(ECG) > 120 ms3/m2 had the sensitivity of 64% for detection of increased LVM. The sensitivities of the other parameters were significantly lower (sensitivity range 18-42%). Relative intra- and interobserver errors and correlation coefficients for LVMI(ECG) calculation were 0.4% and 1.6% and r = 0.94 and 0.98, respectively. CONCLUSIONS: In patients with CAD an assessment of LV mass and detection of hypertrophy using the QRS complex time-dependent index is feasible. The new index correlated well with echocardiographically-determined LVM and showed better statistical performance than indices which include QRS-voltage measurements. The results are promising and warrant further studies to evaluate the utility of the new index as a risk predictor.     

Association of left bundle branch block with left ventricular structure and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Electrocardiographic (ECG) left bundle branch block (LBBB) is associated with left ventricular hypertrophy (LVH), but its relation to left ventricular (LV) geometry and function in hypertensive patients with ECG LVH is unknown. Echocardiograms were performed in 933 patients (548 women, mean age 66+/-7 years) with essential hypertension and LVH by baseline ECG in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. LBBB, defined by Minnesota code 7.1, was present in 47 patients and absent in 886 patients. Patients with and without LBBB were similar in age, gender, body mass index, blood pressure, prevalence of diabetes, and history of myocardial infarction. Despite similarly elevated mean LV mass (126+/-25 vs 124+/-26 g/m(2)) and relative wall thickness (0.41+/-0.07 vs 0.41+/-0.07, P=NS), patients with LBBB had lower LV fractional shortening (30+/-6 vs 34+/-6%), ejection fraction (56+/-10 vs 61+/-8%), midwall shortening (14+/-2 vs 16+/-2%), stress-corrected midwall shortening (90+/-13 vs 97+/-13%) (all P<0.001), and lower LV stroke index (38+/-7 vs 42+/-9 ml/m(2)) (P<0.05). Patients with LBBB also had reduced LV inferior wall and lower mitral E/A ratio (0.75+/-0.18 vs 0.87+/-0.38) (all P<0.05). The above univariate results were confirmed by multivariate analyses adjusted for gender, age, blood pressures, height, weight, body mass index, heart rate, and LV mass index. Among hypertensive patients at high risk because of ECG LVH, the presence of LBBB identifies individuals with worse global and regional LV systolic function and impaired LV relaxation without more severe LVH by echocardiography.     

Geometric determinants of electrocardiographic left ventricular hypertrophy

Experimental studies have suggested that electrocardiographic recognition of left ventricular hypertrophy depends on geometric relationships involving wall thickness and chamber size. To determine the clinical significance of these observations, we studied the effects of echocardiographic LV mass (LVM), posterior wall thickness (PWT), interventricular septal thickness (IVST) and internal dimension (LVID) on ECG voltage in 360 patients. Standard voltage and nonvoltage manifestations of LVH correlated modestly with LVM (r = 0.33-0.44, p less than 0.001). Sokolow-Lyon precordial voltage (SLV) (SV1 + RV5 or V6) correlated moderately with LVM (r = 0.41, p less than 0.001), but correlated less well with IVST (r = 0.26), PWT (r = 0.24) or LVID (r = 0.22). Stepwise regression revealed that there was no relation, independent of LVM, between SLV and IVST (r = 0.03), PWT (r = 0.03) or LVID (r = 0.01). The 90 patients with increased LVM (greater than 215 g) but without LVH by SLV (false negatives) were compared with the 48 identified by SLV (true positives). False negatives differed from true positives in LVM (298 +/- 72 vs 339 +/- 98 g, p less than 0.01), age (55 +/- 18 vs 44 +/- 19 years, p less than 0.001), weight (70 +/- 16 vs 63 +/- 14 kg, p less than 0.02), and distance from skin to the interventricular septum (42 +/- 10 vs 38 +/- 8 mm, p less than 0.02). Thus, for a given LVM, ECG voltage criteria of LVH are independent of LV chamber dilatation or other geometric variables, but depend on age, weight and LV depth in the chest, suggesting that stratification of subjects by clinical variables has promise for improved electrocardiographic recognition of LVH.     

Regression of electrocardiographic left ventricular hypertrophy predicts regression of echocardiographic left ventricular mass: the LIFE study

The electrocardiogram (ECG) is widely used for detection of left ventricular hypertrophy (LVH). However, whether changes in ECG LVH during antihypertensive therapy predict changes in LV mass remains unclear. Baseline and year-1 ECGs and echocardiograms were assessed in 584 hypertensive patients with ECG LVH by Sokolow-Lyon or Cornell voltage-duration product criteria at entry into the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy. A >/=25% decrease in Cornell product defined regression of ECG LVH; a <25% decrease defined no significant regression; and an increase defined progression of ECG LVH. Regression of echocardiographic LVH was defined by a >/=20% reduction in LV mass. After 1 year of therapy, 155 patients (27%) had regression of ECG LVH, 286 (49%) had no significant change, and 143 (25%) had progression of ECG LVH. Compared with patients with progression of ECG LVH, patients with no significant decrease and patients with regression of ECG LVH had stepwise greater absolute decreases in LV mass (-16+/-33 vs -29+/-37 vs -32+/-41 g, P<0.001), greater percent reductions in LV mass (-5.7+/-14.6 vs -11.3+/-13.6 vs -12.3+/-15.6%, P<0.001), and were more likely to decrease LV mass by >/=20% (11.2 vs 24.8 vs 36.1%, P<0.001), even after adjusting for possible effects of baseline and change in systolic and diastolic pressures. Compared with progression of ECG LVH, regression of the Cornell product ECG LVH is associated with greater reduction in LV mass and a greater likelihood of regression of anatomic LVH.     

Effects of nitrendipine on diastolic left ventricular function and hypertrophy in patients with hypertension

To assess the effects of antihypertensive therapy on the heart, left ventricular mass and performance indices (determined by M-mode and pulsed Doppler echocardiography) were compared before and after 4-5 months of nitrendipine therapy in 19 primary hypertensive patients (stage I and II). MAP was reduced from 17.1 +/- 1.7 to 14.5 +/- 1.7 kPa (128.5 +/- 12.7 to 109.0 +/- 13.1 mm Hg), P less than 0.001. The heart rate increased from 68 +/- 8 to 70 +/- 8 beats/min (P greater than 0.05). None of the indices for systolic function (SV, SI, CO, CI, EF, FS) changed significantly (P greater than 0.05). But the indices for diastolic function (RFF, RFR, VLef, IRP, EFv, A/E) improved remarkably (P less than 0.001 or 0.05). Furthermore, a positive correlation between the increasing rate of VLef and decreasing rate of MAP (r = 0.58, P less than 0.005) was noticed. Therefore, the decreasing in arterial pressure is considered as a major relative factor in the improvement of diastolic dysfunction. The patients were divided into two groups according to LVMI: group A, 11 patients with LVMI greater than or equal to 125 g/m2; while group B, 8 patients with LVMI less than 125 g/m2. The LV diastolic relaxation index IRP improved to a greater degree in group B (P less than 0.05), although the reduction of MAP was more markable in group A (P less than 0.05). This means that factors other than arterial pressure may influence the LV diastolic relaxation. In group A, the LVMI decreased from 155.1 +/- 29.9 to 144.4 +/- 33.0 g/m2 (a reduction of 7.0 +/- 9.0%). It suggests that LV hypertrophy can be "reversed" following nitrendipine therapy in some of the hypertensive patients.     

Relation of echocardiographic left ventricular mass and hypertrophy to persistent electrocardiographic left ventricular hypertropy in hypertensive patients: the LIFE study

Background: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) trial used left ventricular hypertrophy (LVH) on a screening ECG to identify patients at high risk for morbid events. Because of regression to the mean, not all patients who met screening criteria had persistent ECG LVH on the ECG performed at study baseline.Methods: The relationship of echocardiographic LV mass and LVH to persistence or loss of ECG LVH between screening and baseline evaluation was examined in 906 hypertensive patients in the LIFE study, who had echocardiograms and additional ECG performed at study baseline. Patients were categorized according to the presence or absence of ECG LVH by Cornell voltage-duration product criteria or Sokolow-Lyon voltage criteria; echocardiographic LVH was defined by LV mass index (LVMI) > 104 g/m² in women and > 116 g/m² in men.Results: A total of 678 patients (75%) had persistent ECG LVH at baseline evaluation. Compared with the 228 patients without ECG LVH on the second ECG by either criterion, the 106 patients with LVH by both Cornell product and Sokolow-Lyon criteria had significantly higher LVMI (140 ± 31 v 114 ± 21 g/m², P < .001) and a higher prevalence of echocardiographic LVH (86% v 55%, P < .001). Patients with ECG LVH on the baseline ECG by either Cornell product criteria (n = 410) or Sokolow-Lyon voltage criteria (n = 162) had intermediate values of LVMI (125 ± 25 and 121 ± 21 g/m²) and prevalences of echocardiographic LVH (78% and 62%). After controlling for possible effects of age, sex, ethnicity, systolic blood pressure, and body mass index, persistence of ECG LVH on the baseline ECG was associated with an increased risk of echocardiographic LVH: compared with patients with neither ECG criteria for LVH, patients with only Sokolow-Lyon voltage criteria had a 1.2-fold increased risk of echocardiographic LVH, those with only Cornell product criteria had a 2.7-fold increased risk, and patients with both ECG criteria had a 4.1-fold increased risk of echocardiographic LVH (P < .001).Conclusions: Persistent ECG LVH between screening and LIFE study baseline identified patients with greater LV mass and a higher prevalence of echocardiographic LVH, suggesting that these patients may be at higher risk for subsequent morbid and mortal events.     

Regression of left ventricular hypertrophy in hypertensive patients treated with indapamide SR 1.5 mg versus enalapril 20 mg: the LIVE study

OBJECTIVE: To compare the efficacy of indapamide sustained release (SR) 1.5 mg and enalapril 20 mg at reducing left ventricular mass index (LVMI) in hypertensive patients with left ventricular hypertrophy (LVH). DESIGN: The LIVE study (left ventricular hypertrophy regression, indapamide versus enalapril) was a 1 year, prospective, randomized, double-blind study. For the first time, a committee validated LVH before inclusion, provided on-going quality control during the study, and performed an end-study reading of all echocardiograms blinded to sequence. SETTING: European hospitals, general practitioners and cardiologists. PATIENTS: Hypertensive patients aged > or = 20 years with LVH (LVMI in men > 120 g/m2; LVMI in women > 100 g/m2). Data were obtained from 411 of 505 randomized patients. INTERVENTIONS: Indapamide SR 1.5 mg, or enalapril 20 mg, daily for 48 weeks. MAIN OUTCOME MEASURES: LVMI variation in the perprotocol population. RESULTS: Indapamide SR 1.5 mg significantly reduced LVMI (-8.4 +/- 30.5 g/m2 from baseline; P< 0.001), but enalapril 20 mg did not (-1.9 +/- 28.3 g/m2). Indapamide SR 1.5 mg reduced LVMI significantly more than enalapril 20 mg: -6.5 g/m2, P = 0.013 (-4.3 g/m2 when adjusted for baseline values; P = 0.049). Both drugs equally and significantly reduced blood pressures (P< 0.001), without correlation with LVMI changes. Indapamide SR progressively reduced wall thicknesses throughout the 1-year treatment period. In contrast, the effect of enalapril observed at 6 months was not maintained at 12 months. CONCLUSIONS: Indapamide SR 1.5 mg was significantly more effective than enalapril 20 mg at reducing LVMI in hypertensive patients with LVH.     

Electrocardiographic diagnosis of left ventricular hypertrophy in the presence of left bundle branch block

The electrocardiographic diagnosis of LVH in the presence of LBBB has previously been difficult. Thirty-seven patients with complete LBBB were identified and had echocardiography performed. Using an accepted echocardiographic formula, left ventricular mass was calculated. Twenty of the 37 patients (54%) were classified as having severe LVH. Multiple conventional ECG criteria for LVH were then evaluated. No QRS voltage criteria showed any difference between patients with and without LVH (P = NS). There was also no correlation between either QRS axis or left atrial enlargement and left ventricular mass (P = NS). However, the QRS duration was significantly longer in the patients with LVH (160 +/- 12 msec) than in the normal patients (148 +/- 11 msec) (P less than 0.001). The sensitivity, specificity, positive predictive value, and accuracy of several voltage criteria and QRS duration were examined. The best voltage criteria had a sensitivity of only 50% and a predictive value of 63%. However, a QRS duration greater than 155 msec had a sensitivity of 60% and a predictive value of 82%. This study demonstrates that the conventional QRS voltage criteria for LVH are not accurate in LBBB. A relationship exists between increasing QRS duration in LBBB and LVH; therefore, the relative probability adjectives: "consider," "possible," and "probable" should be used. QRS duration greater than 155 msec is predictive of LVH despite the presence of LBBB.     

Effects of losartan and atenolol on left ventricular mass and neurohormonal profile in patients with essential hypertension and left ventricular hypertrophy

OBJECTIVE: To compare the effects of the angiotensin II antagonist, losartan, with those of atenolol on left ventricular hypertrophy (LVH), blood pressure and neurohormone concentrations in hypertensive patients with LVH. DESIGN: A multinational, randomized, double-blind trial. SETTING: Hospital. PATIENTS: Hypertensive patients with an echocardiographically documented left ventricular mass index (LVMI) 120 g/m(2) (men) or 105 g/m(2) (women). INTERVENTIONS: Patients allocated randomly to groups received either losartan or atenolol 50 mg/day for 36 weeks, with possible titration to 100 mg/day, and addition of hydrochlorothiazide 12.5 or 25 mg/day. MAIN OUTCOME MEASURES: Changes in LVMI and sitting systolic (SBP) and diastolic (DBP) blood pressures after 36 weeks of treatment (study powered for non-inferiority hypothesis). All echocardiographic data were read in a central laboratory by staff blinded to the treatments and sequence of echocardiographic tapes. RESULTS: The estimated treatment difference between the losartan and atenolol regimens (mean change from baseline at week 36) in LVMI was -2.5 g/m(2) [95% confidence interval (CI) -7.36 to 2.37 g/m(2) ] in favor of losartan, indicating that losartan was significantly non-inferior ( 0.001, non-inferiority limit 8 g/m(2) ) and numerically superior to atenolol in reducing LVMI. The losartan-based regimen significantly reduced LVMI after 36 weeks compared with baseline (-6.56 g/m(2) , 95% CI -10.24 to -2.88 g/m(2) , P<0.001), whereas the atenolol-based regimen had no significant effect (-3.71 g/m, 95% CI -7.75 to 0.32 g/m(2) , P= NS). In a subset of 82 patients, significant changes in serum concentrations of atrial natriuretic peptide, brain natriuretic peptide and immunoreactive amino-terminal pro-brain natriuretic peptide were recorded in losartan-treated ( 0.01) but not atenolol-treated patients. Losartan and atenolol significantly decreased SBP and DBP from baseline after 6, 12, 24 and 36 weeks. The changes from baseline in DBP were greater in the atenolol group at weeks 6 and 36 [difference -2.6 mmHg ( P= 0.016) at week 36]. However, both treatment regimens achieved similar SBP/DBP values at week 36 (141.1 +/- 12.8/86.8 +/- 8.2 mmHg for losartan and 141.4 +/- 17.2/85.0 +/- 10.1 mmHg for atenolol, respectively). Overall, losartan treatment was associated with significantly fewer drug-related clinical adverse events, compared with atenolol (10 and 22%, respectively, P= 0.028). CONCLUSIONS: Both losartan- and atenolol-based regimens effectively decreased blood pressure. Losartan was non-inferior and numerically superior to atenolol in regression of LVH. The reduction in hypertrophy with losartan treatment was accompanied by reductions in circulating concentrations of cardiac natriuretic peptides. Losartan, by specifically blocking angiotensin II, may therefore have effects on the heart beyond those expected from the decrease in blood pressure alone. Losartan was better tolerated than atenolol.     

Enhanced sensitivity to hypoxia-induced diastolic dysfunction in pressure-overload left ventricular hypertrophy in the rat: role of high-energy phosphate depletion

Isolated buffer-perfused rat hearts with pressure-overload hypertrophy develop a greater decrease in left ventricular (LV) diastolic distensibility and a greater impairment in extent of LV relaxation in response to hypoxia than do normal hearts. Using 31P-NMR spectroscopy, we tested the hypothesis that the enhanced susceptibility of hypertrophied hearts to develop hypoxia-induced diastolic dysfunction is due to an accelerated rate of ATP and/or creatine phosphate depletion. Twelve minutes of hypoxia were imposed on isolated isovolumic (balloon-in-left-ventricle) buffer-perfused hearts from 14 rats with pressure-overload hypertrophy (LVH; LV/body wt ratio = 3.43 +/- 17) secondary to hypertension induced by uninephrectomy plus deoxycorticosterone and salt treatment and from 17 age-matched controls (LV/body wt ratio = 2.22 +/- 0.12, p less than 0.001). Coronary artery flow per gram left ventricle was matched in the LVH and control groups during baseline oxygenated conditions and held constant thereafter. Balloon volume was held constant throughout the experiment so that an increase in LV end-diastolic pressure during hypoxia represented a decrease in LV diastolic distensibility. LV systolic pressure was 165 +/- 9 mm Hg in the LVH group compared with 120 +/- 5 mm Hg in the controls during baseline aerobic perfusion (p less than 0.001). LV end-diastolic pressure rose significantly more in response to 12 minutes of hypoxia in the LVH group (12 +/- 1 to 44 +/- 10 mm Hg) than in the controls (12 +/- 1 to 20 +/- 3 mm Hg, p = 0.04). During baseline aerobic conditions, ATP content was the same in the LVH (17.1 +/- 0.5 mumol/g dry LV wt, n = 4) and control (18.8 +/- 0.6 mumol/g dry LV wt, n = 4, p = NS) groups. During hypoxia, ATP declined at the same rate in the LVH and control groups (3.2 +/- 0.5 versus 3.0 +/- 0.5%/min, p = NS) despite the greater rise in end-diastolic pressure in the LVH group. Creatine phosphate content during baseline aerobic perfusion was 14% lower in the LVH group compared with controls, but the rate of creatine phosphate depletion during 12 minutes of hypoxia was the same. During hypoxia, intracellular pH declined modestly and to the same degree in both groups. Thus, the greater susceptibility to hypoxia-induced diastolic dysfunction observed in isolated buffer-perfused hypertrophied rat hearts cannot be explained by an initially lower total ATP content or by an accelerated rate of decline of ATP or creatine phosphate.(ABSTRACT TRUNCATED AT 400 WORDS)     

Echo-Doppler evaluation of diastolic filling in differently induced left ventricular hypertrophy

The study was performed in order to assess whether left ventricular hypertrophy (LVH) (exercise or pressure-overload induced but of a similar extent) may differently affect LV diastolic function. The authors compared LV filling echo-Doppler indexes of 16 male trained rowers (mean left ventricular mass index (LVMI) = 162 +/- 18 g/m2) with those of 34 male patients with secondary LVH, subdivided into two groups according to the extent of LVH (group I, n = 20, with a mean LVMI = 159 + 20 g/m2, and group II, n = 14, with a mean LVMI = 221 +/- 23 g/m2). No abnormalities of LV diastolic filling were observed in the athletes; while in patients with secondary LVH of group I an impairment of the echo-Doppler indexes was detected. A more severe involvement of the diastolic properties was observed in patients with LVH of group II.     

Gender differences in factors influencing electrocardiographic findings of left ventricular hypertrophy in severe aortic stenosis

We investigated gender differences in factors influencing the electrocardiographic (ECG) findings of left ventricular hypertrophy (LVH) in patients with severe aortic stenosis (AS). The functional and geometric responses of the left ventricle to chronic pressure overload, such as hypertension and AS, have been reported to be different between men and women. However, gender differences in the factors influencing the ECG findings of LVH in pressure overload remain unknown. We conducted a retrospective observational study in consecutive patients with severe AS (aortic valve area (AVA) assessed by cardiac catheterization <1.0 cm²) without concomitant significant aortic regurgitation, mitral stenosis and/or regurgitation, conduction disturbance, or myocardial infarction (n = 35 males, 68 females). The ECG criteria were classified into three categories: (1) high voltage by the Sokolow–Lyon index associated with ST-T wave changes (with no digitalis therapy); (2) high voltage alone; and (3) normal. Groups 1 and 2 were defined as LVH on ECG. We compared the ECG findings in relation to the AS severity between genders. Women were older, but there were no significant differences in the prevalence of hypertension, AVA index (AVAI), mean pressure gradient or peak velocity across the AV, LV mass index (LVMI) derived from echocardiography or the distribution of ECG categories between genders. A multiple logistic regression analysis including age, gender, hypertension, AVAI, mean pressure gradient, and LVMI revealed that the LVMI (P = 0.001) and AVAI (P = 0.0434) were significantly related to the distribution of ECG categories. LVMI significantly predicted LVH on ECG in both genders, but AVAI was a predictive factor in only women. ECG LVH in patients with severe AS may be mainly reflected by LVMI in men and by both LVMI and AVAI in women. Factors other than AVA, such as end-stage disease and/or complicating factors such as hypertension, may underlie the observed differences in ECG findings of LVH between men and women.     

Electrocardiographic left ventricular hypertrophy and effects of antihypertensive drug therapy in hypertensive participants in the Multiple Risk Factor Intervention Trial

Data are reported on electrocardiographic left ventricular hypertrophy (ECG LVH) among 8,012 men classified as hypertensive at baseline in the Multiple Risk Factor Intervention Trial. Compared with those allocated to the usual care (UC) control group, men allocated to the special intervention (SI) group experienced a mean reduction of 4 mm Hg in diastolic blood pressure and 7 mm Hg in systolic blood pressure, over 6 years of follow-up. There were 378 new cases of ECG LVH during follow-up; the incidence in the SI group was about 23% less than that in the UC group (4.2 vs 5.4% 2P less than 0.01). Among the 189 men with ECG LVH at baseline, those in the SI group experienced about 24% more annual follow-up visits at which they were free of ECG LVH (4.6 vs 3.7 visits; 2P less than 0.01). This reduced incidence and increased reversal of ECG LVH in the SI group compared with that in the UC group was consistent with significant overall reductions (2P less than 0.001) among SI men in mean wave amplitude in those leads in which voltage is correlated with left ventricular mass (T wave in V1, R wave in aVL and S wave in V3). In SI and UC groups combined, the presence of ECG LVH either at baseline or at follow-up was associated with several-fold increases in death from cardiovascular diseases in general, and death from coronary artery disease in particular.(ABSTRACT TRUNCATED AT 250 WORDS)     

早期纠正贫血对慢性肾衰竭心血管病变影响的多中心临床研究

目的观察早期使用促红细胞生成素治疗贫血对透析前慢性肾衰竭(CRF)患者心血管病变的影响.方法采用多中心、前瞻性、对照临床研究.血肌酐(Scr)在147～400 μmol/L的CRF患者158例,按基线Hb水平分组.将Hb<110 g/L的患者分为2组,(1)治疗组86例,每周接受α-促红细胞生成素100～135 U/kg皮下注射;(2)对照Ⅰ组40例,未接受α-促红细胞生成素治疗;将Hb≥110 g/L的32例患者作为对照Ⅱ组,未接受α-促红细胞生成素治疗.行超声心动图检查,测左心室质量指数(LVMI)、血压等,随访时间2年.结果 3组患者基线临床资料(年龄、性别、原发病、营养状况、高血压的发生率、使用降压药物的种类和数量等)无明显差异(均P>0.05);治疗组、对照Ⅰ组、对照Ⅱ组患者左心室肥厚(LVH)的发生率分别为72.1%、72.5%、59.4%;LVMI与Hb水平呈负相关(r=-0.70, P<0.01),与Scr呈正相关(r=0.64, P<0.05).治疗24个月后,治疗组患者Hb水平较基线时明显上升(P<0.05),LVMI较基线时明显下降(P<0.05),LVH的发生率(55.8%)较治疗前降低16.3%,但平均动脉压、使用降压药物的数量与基线相比无明显差异.对照Ⅰ组与对照Ⅱ组患者Hb逐渐下降,LVMI明显增加,LVH发生率与基线相比明显增高(P<0.05).随访期间,Scr较基线增高1倍的患者比率,治疗组(3.4%)与对照Ⅰ组(15.0%)相比差异有统计学意义(P<0.05),而对照Ⅰ组与对照Ⅱ组(9.4%)相比无明显差异(P>0.05).结论轻中度CRF患者存在LVH,贫血是导致透析前CRF患者LVH的重要原因.用促红细胞生成素早期治疗贫血能使部分患者LVH逆转.透析前CRF患者用促红细胞生成素治疗并不加重高血压,并可能有助于延缓肾衰竭的进程.     

Long-term effects of balloon angioplasty on left ventricular hypertrophy in adolescent and adult patients with native coarctation of the aorta. Up to 18 years follow-up results.

BACKGROUND: Little is known regarding the long-term follow-up results of balloon angioplasty (BA) for patients with native aortic coarctation (AC) on left ventricular hypertrophy (LVH) regression. OBJECTIVES: The purpose of this study was to define the long-term effect of BA of AC on LVH in adolescent and adult patients. METHODS: Follow-up data of 53 patients (36 male) mean age 24 +/- 9 years undergoing BA for discrete AC at median interval of 11.8 years (range 4-18 years) including cardiac catheterization, magnetic resonance imaging, and Echocardiography form the basis of this study. Patients were divided into two groups at 1 year after BA based on absence (group A) or presence (group B) of persistent hypertension and need for medication. RESULTS: Forty-nine patients had baseline LVH, BA produced an immediate reduction in peak AC gradient from 66 +/- 23 mm Hg (95% confidence interval [CI]: 59.5-72.7) to 10.8 +/- 7 mm Hg (95% CI: 8.8-12.5) (P < 0.0001). Follow-up catheterization 12 months later revealed a residual gradient of 6.2 +/- 6 mm Hg (95% CI: 4.4-7.9) (P < 0.001). The blood pressure had normalized without medication in 38 of the 49 patients (165 +/- 17 to 115 +/- 10 mm Hg). Left ventricular mass index (LVMI) decreased significantly (>20% decrease LVMI from baseline) in 48 patients (98%) at median interval 1.4 years (range 0.5-3 years) post BA, group A (38 patients) LVMI decreased from 132 +/- 30.7 g/m(2) (95% CI: 122-141.9) to 86 +/- 19.9 g/m(2) (95% CI: 79.5-92.5) (P < 0.0001). Similarly, in 10 patients (group B) the LVMI decreased from 157 +/- 38.7 g/m(2) (95% CI: 127-185) to 102 +/- 29 g/m(2) (95% CI: 105-151) (P < 0.0001) at follow-up. Mild (<20% decrease in LVMI) regressions were noted in one patient from group B. There was no progression to LVH in the four patients who had normal baseline LVMI. CONCLUSION: (1) Long-term results of BA for discrete AC are excellent and should be considered as first option for treatment of this disease; (2) Regression of LVH (> or =20% reduction in LVMI) occurred in 98% of patients after BA.     

The degree of albuminuria is related to left ventricular hypertrophy in hypertensive diabetics and is associated with abnormal left ventricular filling: a pilot study

The association of albuminuria and left ventricular (LV) hypertrophy (LVH) in diabetics aggravates the prognosis. The authors studied the relation between LVH and the degree of albuminuria in diabetics and investigated the relationship of albuminuria to LV filling. A comparison was made between 30 hypertensive diabetics, 10 of whom had microalbuminuria (MIC) and 20 had macroalbuminuria (MAC), and 18 diabetics who were normotensive and normalbuminuric (NOR). LV mass index (LVMI) and LV ejection fraction (LVEF) were measured during echocardiography. LV filling pattern at rest and at peak standardized isometric exercise (IME) using handgrip was assessed by measuring E/A (peak velocity of the early/atrial filling waves) of the transmitral flow during Doppler and echocardiography. Each patient underwent a stress ECG test. LVMI was higher in MAC (132.3 +/- 55.4) than in MIC (115.6 +/- 32.5) or NOR (90.0 +/- 31.8) (p<0.01). There were more patients in MAC with LVH (n = 13) and abnormal filling (n = 9 at rest and 16 with IME) than in MIC (LVH = 5, abnormal filling = 1 at rest and 10 during IME) or NOR (LVH = 3, abnormal filling = 1 at rest and 9 during IME) (p < 0.02). LVMI was not related to LVEF. Although blood pressure was not different between MAC and MIC groups, it was significantly higher than in the NOR group. This study suggests that a high degree of albuminuria in hypertensive diabetics is associated with greater value for LVMI and an increased incidence of LVH independent of blood pressure level or systolic LV function. LVH is associated with abnormal LV filling. The degree of albuminuria may predict LVMI and LVH, which are associated with abnormal LV filling. This association of abnormal LV filling with albuminuria in hypertensive diabetic patients may account for their high risk of cardiovascular events.     

Ethnic differences in electrocardiographic criteria for left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint

BACKGROUND: African Americans have greater precordial QRS voltages than whites, with concomitant higher prevalences of electrocardiographic (ECG) left ventricular hypertrophy (LVH) and lower specificity of ECG LVH criteria for the identification of anatomic hypertrophy. However, the high mortality associated with LVH in African American patients makes more accurate ECG detection of LVH in these patients a clinical priority. METHODS: Electrocardiograms and echocardiograms were obtained at study baseline in 120 African American and 751 white hypertensive patients enrolled in the Losartan Intervention For Endpoint (LIFE) echocardiographic substudy. The ECG LVH was determined using Sokolow-Lyon, 12-lead sum, and Cornell voltage criteria. Echocardiographic LVH was defined by LV mass indexed to height(2.7) >46.7 g/m(2.7) in women and >49.1 g/m(2.7) in men. RESULTS: After adjusting for ethnic differences in LV mass, body mass index, sex, and prevalence of diabetes, mean Sokolow-Lyon and 12-lead sum of voltage were significantly higher, but Cornell voltage was lower, in African Americans than in whites. As a consequence of these differences, when identical partition values were used in both ethnic groups, Sokolow-Lyon and 12-lead voltage criteria had lower specificity in African Americans than whites (44% v 69%, P = .007 and 44% v 59%, P = .10) but had greater sensitivity in African Americans (51% v 27%, P < .001 and 62% v 45%, P = .003). In contrast, Cornell voltage specificity was higher (78% v 62%, P = .09) but sensitivity was slightly lower (49% v 57%, P = 0.16) in African Americans. However, when overall test performance was compared using receiver operating curve analyses that were independent of partition value selection, ethnic differences in test performance disappeared, with no differences in accuracy of any of the ECG voltage criteria for the identification of LVH between African American and white hypertensive individuals. CONCLUSIONS: When standard, non-ethnicity-specific thresholds for the identification of LVH are used, Sokolow-Lyon and 12-lead voltage overestimate and Cornell voltage underestimates the presence and severity of LVH in African American relative to white individuals. However, these apparent ethnic differences in test performance disappear when ethnic differences in the distribution of ECG LVH criteria are taken into account. These findings demonstrate that ethnicity-specific ECG criteria can equalize detection of anatomic LVH in African American and white patients.     

Gender differences in regression of electrocardiographic left ventricular hypertrophy during antihypertensive therapy

Although men and women differ in the magnitude of ECG left ventricular hypertrophy, whether gender differences exist in the degree of regression of ECG left ventricular hypertrophy during antihypertensive therapy is unclear. ECG left ventricular hypertrophy defined using gender-adjusted Cornell product and Sokolow-Lyon voltage criteria was assessed serially in 9193 hypertensive patients treated with losartan- or atenolol-based regimens. Changes in ECG left ventricular hypertrophy were measured from baseline to last in-study visit, and above-average regression of hypertrophy was identified by a >or=236-mm . ms reduction in Cornell product or >or=3.5-mm reduction in Sokolow-Lyon voltage. During mean follow-up of 4.8+/-0.9 years, women had less reduction in Cornell product (-149+/-823 versus -251+/-890 mm . ms) and Sokolow-Lyon voltage (-3.0+/-6.8 versus -4.8+/-7.7 mm) than men (both P<0.001). After adjusting for baseline ECG left ventricular hypertrophy levels, baseline and change in systolic and diastolic pressures, treatment group, age, and other baseline gender differences, women had significantly less reduction in both Cornell product (adjusted means: -137 versus -276 mm . ms; P<0.001) and Sokolow-Lyon voltage (-3.6 versus -4.1 mm; P=0.005) than men and were 32% less likely to have had greater than the median level of regression of Cornell product left ventricular hypertrophy (95% CI: 24% to 39%; P<0.001) and 15% less likely to have had regression of left ventricular hypertrophy by Sokolow-Lyon criteria (95% CI: 5% to 23%; P=0.003). Thus, women have less regression of ECG left ventricular hypertrophy than men in response to antihypertensive therapy, independent of baseline gender differences in the severity of ECG left ventricular hypertrophy and after taking into account treatment effects and blood pressure changes.     

Relationship of the electrocardiographic strain pattern to left ventricular structure and function in hypertensive patients: the LIFE study. Losartan Intervention For End point

OBJECTIVES: This study was designed to assess the relation of electrocardiographic (ECG) strain to increased left ventricular (LV) mass, independent of its relation to coronary heart disease (CHD). BACKGROUND: The classic ECG strain pattern, ST depression and T-wave inversion, is a marker for left ventricular hypertrophy (LVH) and adverse prognosis. However, the independence of the relation of strain to increased LV mass from its relation to CHD has not been extensively examined. METHODS: Electrocardiograms and echocardiograms were examined at study baseline in 886 hypertensive patients with ECG LVH by Cornell voltage-duration product and/or Sokolow-Lyon voltage enrolled in the Losartan Intervention For End point (LIFE) echocardiographic substudy. Strain was defined as a downsloping convex ST segment with inverted asymmetrical T-wave opposite to the QRS axis in leads V5 and/or V6. RESULTS: Strain occurred in 15% of patients, more commonly in patients with than without evident CHD (29%, 51/175 vs. 11%, 81/711, p < 0.001). When differences in gender, race, diabetes, systolic pressure, serum creatinine and high density lipoprotein cholesterol were controlled, strain on baseline ECG was associated with greater indexed LV mass in patients with (152 +/- 33 vs. 131 +/- 32 g/m2, p < 0.001) or without CHD (131 +/- 24 vs. 119 +/- 22 g/m2, p < 0.001). In logistic regression analyses, strain was associated with an increased risk of anatomic LVH in patients with CHD (relative risk 5.14, 95% confidence interval [CI] 1.16 to 22.85, p = 0.0315), without evident CHD (relative risk 2.91, 95% CI 1.50 to 5.65, p = 0.0016), and in the overall population when CHD was taken into account (relative risk 2.98, 95% CI 1.65 to 5.38, p = 0.0003). CONCLUSIONS: When clinical evidence of CHD is accounted for, ECG strain is likely to indicate the presence of anatomic LVH. Greater LV mass and higher prevalence of LVH in patients with strain offer insights into the known association of the strain pattern with adverse outcomes.