Reversal of left ventricular hypertrophy with captopril: Heterogeneity of response among hypertensive patients

Reversal of left ventricular hypertrophy (LVH) has been reported not to occur with all antihypertensive agents. Moreover, a dissociation between blood pressure response to medical therapy and reversal of ventricular hypertrophy has been previously observed. To evaluate the effects of captopril we studied the electrocardiographic (ECG) changes in 26 severe hypertensive patients who received the drug for more than one year. In 14 patients with normal pretreatment ECG, captopril controlled blood pressure effectively [132±2.9 (SE) to 104±3.9 mmHg, p<0.001], but had no effect on ECG voltage. In 12 patients with pretreatment LVH, two different response patterns were observed despite similar blood pressure control (144±4.9 to 102±3.1 mmHg and 148±7.3 to 109±7.3 mmHg, p<0.001 for both): seven had complete normalization of ECG while five had residual LVH pattern. No significant difference was found between the latter two groups in regard to age, sex, weight, etiology of hypertension, pretreatment ECG voltage, blood pressure, plasma renin activity, duration of treatment and duration of maintained blood pressure control. The reversal of LVH pattern occurred early (between 12 to 16 months) with no overall correlation between lowering of blood pressure and ECG voltage changes. The heterogeneity of response observed in this study suggests that factors other than blood pressure control modify the reversal of cardiac hypertrophy by antihypertensive therapy.     

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.     

Regression of left ventricular hypertrophy and prevention of left ventricular dysfunction by captopril in the spontaneously hypertensive rat.

To determine whether chronic antihypertensive therapy prevents the progression of cardiac hypertrophy and the deterioration in cardiac performance observed in spontaneously hypertensive rats (SHR) with long-term hypertension, 14-month-old female SHR and normotensive American Wistar rats (NWR) were treated for 10 months with an inhibitor of angiotensin I-converting enzyme, captopril (2 g/liter of drinking water). Captopril reduced the marked left ventricular hypertrophy of 24-month-old SHR (untreated, 4.37 +/- 0.2 mg/g of body weight; treated, 3.01 +/- 0.1 mg/g; P less than 0.02) to levels observed in 6-month-old SHR. Treatment prevented the reductions in baseline and maximal aortic blood flows that occurred in SHR between ages 12 and 24 months yet had no effect on the blood flows of NWR. The diminished maximal stroke volume of untreated SHR was ejected from a significantly increased left ventricular end-diastolic volume, so that the ejection-fraction index was markedly reduced (24-month-old untreated NWR, 84 +/- 3%; untreated SHR, 56 +/- 5%; P less than 0.001). Therapy restores this index in SHR to normal (77 +/- 4%). The relationship between ejection-fraction index, and afterload was also normal in treated SHR. Thus, chronic therapy with captopril produced a marked regression of cardiac hypertrophy and prevented the deterioration of cardiac performance in SHR with long-standing hypertension.     

ECG alterations with progressive left ventricular hypertrophy in spontaneous hypertension.

Although many ECG criteria exist for diagnosis of left ventricular hypertrophy (LVH) in hypertensive man, little is known of which specific ECG changes accompany progression of LVH with duration of hypertension. The spontaneously hypertensive rat (SHR) provides the best animal model thus far developed for studying this process since these animals demonstrate a progressive increase in left ventricular/body weight ratio with age. Electrocardiograms were performed under light ether anesthesia in four age groups of SHR and two normotensive Wistar strains (NR and WKY). Analysis of variance for two factors (rat strain and age) revealed progressively increased QRS and P-wave duration and delay in intrinsicoid deflection in SHR (p less than 0.001). Bipeak P-wave notching was also noted in SHR similar to left atrial abnormality in hypertensive man. Thus, specific ECG indices can be identified in association with the known progressive increase in left ventricular mass in SHR and should provide a better means to understand evolving ECG changes in LVH.     

Metabolic, hemodynamic, and cardiac effects of captopril in young, spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) demonstrate elevated blood pressure, cardiac hypertrophy, glucose intolerance, and insulin resistance compared with age-matched Wistar-Kyoto rats (WKY). We investigated concurrent effects of captopril on blood pressure, cardiac mass, myocardial enzyme activities, glucose tolerance, and insulin action in young male SHR. At 10 weeks of age, SHR were randomized into two groups, one receiving distilled water, the other a captopril solution (50 mg/kg body weight/day). We also examined age-matched WKY receiving distilled water. Blood pressure was measured by tail-cuff during the 4-week treatment period and oral glucose tolerance was tested at the end of treatment. Hearts were weighed and ventricular tissue was assayed for activities of 3-hydroxyacyl-CoA dehydrogenase, citrate synthase, and hexokinase. Growth rates were similar between captopril-treated and control SHR, but less than those of WKY. Captopril reduced blood pressure (134 +/- 8 v 177 +/- 8 mm Hg, P < .05) and left ventricular mass (-18%, P < .05) in SHR. Cardiac enzyme activities also changed with captopril treatment, reflecting an increased capacity for beta-oxidation of fatty acids and reduced potential for glucose phosphorylation in the left ventricle of SHR. Serum concentrations of glucose, insulin, and free fatty acids after a brief fast and in response to oral glucose were not different after captopril treatment, suggesting no improvement in insulin action or glucose tolerance. In summary, treatment of young male SHR with captopril reduces blood pressure and cardiac mass, and promotes a small but significant increase in cardiac capacity for oxidation of fatty acids and reduction of glucose phosphorylation. In contrast, metabolic effects of captopril on oral glucose tolerance and insulin action were not evident.     

Prolonged QT Interval Is Associated with Blood Pressure Rather Than Left Ventricular Mass in Spontaneously Hypertensive Rats

QT interval is prolonged in hypertensive individuals, although the factors responsible for this increase are not completely understood. We questioned whether enhanced left ventricular mass (LVM) or increased systemic blood pressure represents the principal factor determining QT prolongation in the period of development of hypertension and left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR). In 12-and 20-week-old SHR (SHR12 and SHR20) and age-matched normotensive Wistar-Kyoto rats (WKY12 and WKY20), arterial systolic blood pressure (sBP) was measured using tail-cuff technique. Orthogonal Frank ECG was registered in anaesthetized animals in vivo, and bipolar ECG was measured in spontaneously beating isolated hearts in vitro. Progressive increase of sBP and LVM resulted in significant QT prolongation in SHR20 as compared to WKY12, WKY20, and also to SHR12 in vivo (WKY12: 82?±?9 ms, WKY20: 81?±?9 ms, SHR12: 88?±?15 and SHR20: 100?±?10, respectively; p?<?0.05) but not in isolated hearts (WKY20: 196?±?39 ms and SHR20: 220?±?55, respectively; NS). In whole animals, QT duration was positively related to sBP (r?=?0.6842; p?<?0.001) but not to LVM (r?=?0.1632, NS) in SHR20. The results suggest that QT prolongation in SHR developing hypertension and LVH depends on blood pressure rather than increase in LVM. In this period, myocardial hypertrophy is probably the predisposition for QT prolongation, but the significant change manifests only in the presence of elevated systemic factors.     

The Initial Stage of Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats is Manifested by a Decrease in the QRS Amplitude/Left Ventricular Mass Ratio

In this study we tested the hypothesis of the relative voltage deficit, i.e. the discrepancy between increased left ventricular mass (LVM) and QRS amplitudes, in an experimental model of spontaneously hypertensive rats (SHR) during the period of a moderate increase in blood pressure. To address this issue we recorded orthogonal electrocardiograms of male SHR at the age of 12 and 20 weeks. During this period the systolic blood pressure (sBP) increased from 165 ± 3 mmHg to 195 ± 1 mmHg (p < 0.001). Age and sex matched WKY rats were used as control groups. The sBP values in WKY normotensive control groups were within normal limits (122 ± 8 mmHg and 130 ± 4mmHg, respectively). The maximum QRS spatial vector magnitude (QRSmax) was calculated from X, Y, Z amplitudes of the orthogonal electrocardiograms. The animals were sacrificed and the left ventricular mass was weight. The specific potential of myocardium (SP) was calculated as a ratio of QRSmax to LVM. The LVM in SHR (0.86 ± 0.05 g and 1.05 ± 0.07 g, respectively) was significantly higher as compared to WKY (0.65 ± 0.07 g and 0.70 ± 0.02 g), and the increase of LVM closely correlated with the sBP increase. On the other hand, QRSmax in SHR did not follow either the increase of sBP, or LVM. The QRSmax values in SHR did not differ from those of WKY at the age of 12 weeks (0.59 ± 0.14 mV compared to 0.46 ± 0.05 mV), and they were even lower in SHR at the age of 20 weeks (0.74 ± 0.08 mV compared to 0.44 ± 0.05 mV, p < 0.001). The values of SP, quantifying the relative voltage deficit, were significantly lower in SHR as compared to the WKY control. The values decreased significantly in SHR with increasing age, sBP and LVM, i.e., with the progression of hypertrophic remodeling of the left ventricle. The results of this study support the hypothesis of the relative voltage deficit in LVH. These results are consistent with the finding of a high number of false negative ECG results in clinical ECG diagnostics of LVH, and could contribute to an understanding of the diagnostic importance of the false negative ECG results, their re‐evaluation and utilization for clinical diagnosis and prognosis.     

高血压大鼠左室肥厚消退后的心电活动变化

用尼群地平、卡托普利治疗自发性高血压大鼠，逆转其左室肥厚，比较左室肥厚消退前后心电活动变化。结果发现，两药均可使左室肥厚消退，与同周龄自发性高血压大鼠相比，两药物治疗组单相动作电位复极化９０％时程（ｍｓ）缩短（分别为８７±９ＶＳ１０４±１４；９０±９ＶＳ１０４±１４，Ｐ均＜０．０５），室颤阈值（ｍＡ）提高（分别为１６．７５±４．４３ＶＳ８．７５±３．８８；２０．００±５．４０ＶＳ８．７５±３．８８，Ｐ均＜０．０５），氯化铯诱发心律失常的发生率降低，各指标值与同周龄ＷＫｙ鼠相近。表明随着左室肥厚消退，心电活动异常也得到改善。     

Beneficial effects of 1-year captopril therapy in children with chronic aortic regurgitation who have no symptoms

Objective This prospective study was performed to assess the effects of 1 year of angiotensin-converting enzyme inhibition with captopril in 20 children (mean age 14.3 ± 2.3 years) with asymptomatic chronic aortic regurgitation. Methods and Results At 12 months patients receiving captopril had a significant reduction in left ventricular end-diastolic and end-systolic dimensions (57 ± 9.3 vs 51 ± 9.5 mm, p < 0.001; 35.4 ± 6.1 vs 32 ± 6.8 mm, p < 0.001), end-diastolic and end-systolic volume indexes (111 ± 36 vs 94 ± 29 ml/m², p < 0.001; 35 ± 13 vs 30 ± 12 ml/m², p < 0.001, respectively), and mass index (138 ± 37 vs 109 ± 32 gm/m², p < 0.0001) determined by two-dimensional echocardiography. Meridian (p < 0.01) and circumferential (p < 0.0001) wall stresses also decreased significantly with therapy. Significant reduction (27.8%, p < 0.0001) was achieved in regurgitant fraction with captopril. Conclusions These data show that the long-term therapy with angiotensin-converting enzyme inhibitors is able to reverse left ventricular dilation and hypertrophy and suggest that such therapy has the potential to favorably influence the natural history of the disease in children. (Am Heart J 1998;135:598-603.)     

复方降压片对高血压大鼠冠状动脉壁肥厚和储备力下降的影响

目的 研究复方降压片对高血压大鼠冠状动脉壁肥厚和储备力下降的影响。方法 4w大鼠设4组：分别为自发性高血压大鼠(SHR)组、SHR口服复方降压片组、SHR口服卡托普利组和正常血压大鼠(WKY)组，饲养12w。冠脉最大血流量用离体心脏灌注法测定。结果 复方降压片能显著降低SHR收缩压、冠状动脉横截面积，提高最大冠状动脉流量，与卡托普利相似。复方降压片能降低SHR的左心室重与体重比，但仍然显著高于WKY组和口服卡托普利组。结论 复方降压片能预防SHR冠状动脉壁肥厚、储备力下降，减轻左心室肥厚；冠状动脉血流储备力的损害程度和左心室肥厚程度不平行。     

Angiotensin-converting enzyme inhibition and beta-adrenoceptor blockade regress established ventricular remodeling in a canine model of discrete myocardial damage

Objectives. This study was designed to assess the effect of angiotensin-converting enzyme inhibition and beta-adrenoreceptor blockade on established ventricular remodeling.Background. Angiotensin-converting enzyme inhibitor therapy attenuates the development of ventricular remodeling when given shortly after myocardial infarction. However, regression of established ventricular remodeling after infarction has received little attention.Methods. The relative effects of angiotensin-converting enzyme inhibitor therapy and beta-adrenoceptor blockade on established ventricular remodeling were assessed in a canine model characterized by increased left ventricular mass and chamber dilation as a result of localized myocardial necrosis produced by transmyocardial direct current shock. Dogs were randomly assigned to 3 months of therapy with captopril (25 mg twice daily, n = 7) or metoprolol (100 mg twice daily, n = 7) or to a control group with no intervention (n = 6), 11 ± 4 (mean ± SD) months after acute myocardial damage.Results. Compared with the control group, dogs in both the captopril and metoprolol groups had reduced left ventricular mass as measured by magnetic resonance imaging (−8.1 ± 3.8 vs. 1.7 ± 2.8 g, p = 0.003 and −9.6 ± 5.6 vs. 1.7 ± 2.8 g, p = 0.001), respectively. Captopril and metoprolol also produced a reduction in left ventricular end-diastolic volume (−7.6 ± 6.0 and −6.0 ± 5.8 ml, respectively) compared with the control value (−1.6 ± 3.8 ml) (p = 0.14 [NS]). Both agents reduced mean arterial pressure but had disparate effects on pulmonary wedge pressure and right atrial pressure. There was no significant correlation between change in ventricular mass or volume and change in any measured hemodynamic or neurohormonal variable.Conclusions. These data suggest that pharmacologic intervention with angiotensin-converting enzyme inhibition or betaadrenoceptor blockade can result in regression of established ventricular remodeling. The mechanism of this response will require further study, but these data did not support a close association between regression of remodeling and hemodynamic unloading of the ventricle or systemic neuroendocrine factors.     

Effects of blood pressure changes on development and regression of electrocardiographic left ventricular hypertrophy: a 26 year longitudinal study

At the Radiation Effects Research Foundation, medical examinations have been conducted biennially since 1958 on a fixed population of approximately 20,000 individuals. Blood pressure measurements and electrocardiographic (ECG) recordings are available for 6,569 individuals who were monitored for at least 11 of the 13 2 year intervals between 1958 and 1984. Data from 601 individuals who had satisfied the Foundation's ECG diagnostic criteria of left ventricular hypertrophy ("Kagan-Yano code") on at least one occasion were reviewed. Both the development and the regression of ECG left ventricular hypertrophy were ascertained in 61 subjects (17 men and 44 women). During the course of development of ECG left ventricular hypertrophy, hypertension (including borderline cases) was noted in 83.3% of the subjects. The most common pattern of ECG left ventricular hypertrophy development was high voltage, followed by ST-T changes. In about half of these cases, the condition of hypertrophy regression was associated with lowering of blood pressure, marked by the disappearance of high voltage ECG readings.     

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.     

Vasodilator therapy in chronic asymptomatic aortic regurgitation: Enalapril versus hydralazine therapy

Objectives. This study attempted to evaluate the long-term effcacy of enalapril versus hydralazine therapy on left ventricular volume, mass and function as well as on the renin-angiotensin system in chronic asymptomatic aortic regurgitation.Background. We tested the hypothesis that early administration of a vasodilator drag might be able to reduce left ventricular dilution and mass expansion. Because the renin-angiotensin system may be activated in chronic aortic regurgitation, early enalapril therapy might be beneficial.Methods. Between 1990 and 1993, 76 asymptomatic nonrheumatic patients with mild to severe chronic aortic regurgitation were enrolled in a randomized, double-blind trial comparing enalapril with hydralazine. All patients underwent serial noninvasive studies. Seventy patients completed the 12-month follow-up.Results. At 1 year, patients receiving enalapril had a significant reduction in left ventricular end-diastolic and end-systolic volume indexes (124 ± 15 vs. 108 ± 17 ml/m², p < 0.01; 50 ± 12 vs. 40 ± 14 ml/m², p < 0.01, respectively) and mass index (131 ± 16 vs. 113 ± 19 g/m², p < 0.01), wheress hydralazine therapy showed no significant changes. Both regimens not only had a significant reduction in left ventricular mean wall stress but also had a mild increase in exercise duration. Only enalapril therapy achieved a significant inhibition of the renin-angiotensin system, in contrast to hydralazine therapy. Moreover, the multiple r²value from the analysis for end-diastolic volume index using the two variables of age and treatment drugs was 72.1% (p < 0.01).Conclusions. Both regimens decrease left ventricular mean wall stress. Enalapril therapy achieves significant left ventricular mass regression, left ventricular end-diastolic and end-systolic volume index reduction and renin-angiotensin system suppression. These findings suggest that early unloading enalapril therapy has the potential to favorably influence the natural history of chronic aortic regurgitation.     

卡维地洛长期治疗对原发性高血压左心室肥厚及室性心律失常干预的对比研究

目的探讨β及α受体阻滞剂卡维地洛对原发性高血压(EH)患者左心室肥厚(LVH)及室性心律失常(VA)的干预作用。方法入选经超声心动图、心电图、动态心电图检查证实为EH伴LVH及VA患者72例,随机分配到卡维地洛组(口服25~50mg/d)或卡托普利组(口服25~75mg/d),治疗8个月,治疗前后各检查超声心动图、心电图、动态心电图,对比分析组内治疗前后左心室重量指数及VA变化和两组间的差异。结果①与治疗前比较,EH患者在卡维地洛或卡托普利治疗8个月后,两组收缩压与舒张压明显下降(166/104mmHg至135/86mmHg;162/103mmHg至138/87mmHg)(P均<0.01)。②卡维地洛组治疗后,左心室后壁与室间隔厚度较治疗前显著下降(P<0.05),左心室重量及左心室重量指数下降更显著(P均<0.01);卡托普利组治疗后左心室后壁与室间隔厚度及左心室重量及左心室重量指数下降显著(P均<0.05)。③卡维地洛组治疗后VA及复杂性室性VA的控制率为91.67%(33/36);卡托普利组治疗后VA及复杂性VA的控制率为36.1%(13/36),两组间差异有显著性(P<0.01)。结论EH伴LVH及VA患者在卡维地洛治疗8个月后LVH显著逆转,卡维地洛对VA的干预明显优于卡托普利。     

非降压剂量血管紧张素转换酶抑制剂对高血压冠状动脉肥厚的影响

目的　研究非降压剂量的血管紧张素转换酶抑制剂 (ACEI)对高血压冠状动脉肥厚的影响。方法 16周大鼠设4组 (各组n =6 ) :分别为自发性高血压大鼠 (SHR)组、SHR口服降压剂量卡托普利组 (40mg·kg- 1 ·d- 1 )、SHR口服非降压剂量卡托普利组 (2mg·kg- 1 ·d - 1 )和正常血压大鼠 (WKY)组 ,饲养 10周。结果　降压剂量卡托普利治疗显著降低SHR的收缩压 ,非降压剂量卡托普利治疗不降低SHR的收缩压 ;降压和非降压剂量卡托普利都显著减少了SHR冠状动脉壁横截面积、横截面积 内径比 ,减轻SHR冠状动脉前降支中层血管平滑肌细胞的肥大 ,都显著提高SHR的最大冠状动脉流量。结论　ACEI治疗对冠状动脉肥厚的逆转作用和对冠状动脉功能的改善作用可以不依赖于血压下降的效果 ,临床上应用ACEI降压不明显的病人继续使用ACEI可能有助于逆转血管壁肥厚 ,改善血管功能。     

Serial noninvasive assessment of left ventricular hypertrophy and function after surgical correction of aortic regurgitation.

Serial echocardiographic analyses of left ventricular hypertrophy and function, with validation of extent of shortening by first pass radionuclide angiography, was performed in 16 patients before and after surgical correction of severe aortic valve regurgitation. All patients were symptomatic (predominantly in New York Heart Association functional class III or IV) before operation but were in class I or II after operation. The preoperative pattern of eccentric hypertrophy (increased mass with normal ratio of left ventricular cross-sectional wall area to cavity area) changed immediately after operation to a pattern of concentric hypertrophy (increased mass with increased ratio of left ventricular cross-sectional wall area to cavity area) because of a significant reduction in chamber size and increase in wall thickness. On late follow-up (9 to 35 months, average 15 months after operation), the hypertrophy lessened significantly, the cross-sectional area of the ventricular wall decreasing to 21.1 ± 5.4 (mean ± standard deviation) cm² from a preoperative average of 31.6 ± 4.8 cm² (P < 0.01), and the ratio of wall area to cavity area was once again normal. In the same period, left ventricular enddiastolic diameter decreased from 6.52 ± 0.68 to 4.64 ± 0.52 cm (P < 0.01). Preoperatively, ejection phase indexes were normal or only marginally depressed in 12 of 16 patients but were moderately depressed in the remaining 4. At early follow-up (average 4 months) ventricular shortening tended to increase; and at late follow-up the fractional shortening of the minor axis, the ejection fraction and the mean velocity of circumferential fiber shortening increased to 0.39 ± 0.07, 0.68 ± 0.10 and 1.26 ± 0.22 circumference/sec, respectively, from preoperative values of 0.33 ± 0.09, 0.60 ± 0.14 and 1.05 ± 0.31 circumferences/sec (P < 0.05 for each index). In the four subjects with preoperative depression of left ventricular function, the extent and speed of myocardial shortening at late follow-up became normal in three subjects and remained moderately depressed in one patient. Paradoxical septal motion was observed immediately postoperatively and in the early follow-up studies, but it was noted in only 3 of 16 cases by the late follow-up period. Provided septal dyskinesia was not present, echocardiographic and first pass radionuclide determinations of ejection fraction correlated highly (r = 0.92).It is concluded that when aortic valve replacement for symptomatic aortic regurgitation is undertaken prior to severe myocardial decompensation, improvement in clinical status is associated with significant regression of myocardial hypertrophy, reduction in left ventricular size, evolution of a normal $\text{mass}\text{volume}$ ratio, recovery of septal dyskinesia as revealed on echocardiography, and improvement in left ventricular function. These data do not define the type and degree of left ventricular dysfunction which is irreversible.     

Pumping ability of the hypertrophying left ventricle of the spontaneously hypertensive rat.

Cardiac pumping ability was assessed during the natural development of left ventricular hypertrophy by elevating venous pressure by infusing Tyrode's solution intravenously to produce peak cardiac output. This experiment was performed on spontaneously hypertensive rats (SHR) of three age groups (11, 24, and 83 weeks). From 11 to 24 weeks, peak cardiac output of SHR increased in direct proportion to the abnormally increased ventricular mass; Thus peak cardiac output per gram of left ventricle (LV) remained stable. Similar results were obtained for two strains of normotensive rats at each of the same three age groups. Thus, in the normotensive animal peak cardiac output per gram of LV remained stable over a wide range of ages and varying left ventricular weights. However, with progressive elevation of arterial pressure in aging SHR (83 weeks), we observed severe ventricular hypertrophy (100% increases in left ventricular to body weight ratio). In this oldest SHR group, unlike age-matched normotensive rats, there was a marked reduction in the pumping ability per gram of LV. Thus, during the natural development of left ventricular hypertrophy SHR demonstrated both a stable stage of hypertrophy in which the increased left ventricular mass maintained its pumping ability, and a later stage of deterioration in which there was a loss of the normal relationship between ventricular mass and pumping ability.     

潜阳通络方对肝阳上亢证自发性高血压大鼠左室肥厚及儿茶酚胺的影响

目的观察潜阳通络方对肝阳上亢证自发性高血压大鼠(SHR)左室肥厚(LVH)及儿茶酚胺(CA)的影响。方法用32只14周龄SHR大鼠,随机分为模型组、潜阳通络方低剂量组、潜阳通络方高剂量组和卡托普利。另购8只14周龄雄性Wistar大鼠,为空白对照组。参照相关文献,将SHR大鼠加灌附子汤法造肝阳上亢模型,实验期间每周末测量血压,实验结束后取材,测量左室重量及CA含量。结果对治疗结束后,与模型组血压相比,其余各治疗组血压均有显著下降(P<0.01),且三组之间相比较,也均有显著性差异(P<0.01)与模型组左室重量指数(LVMI)比较,潜阳通络方高、低剂量组LVMI均有显著性降低(P<0.05),卡托普利组与模型组比较,无显著变化(P>0.05)。与模型组肾上腺素(AD)比较,其余各治疗组AD含量均明显降低(P<0.05),但三组之间差异不显著。与模型组去甲肾上腺素(NE)比较,其余各治疗组NE含量均明显降低(P<0.05),且潜阳通络方高、低剂量组与卡托普利组差异显著(P<0.05),潜阳通络方低、高剂量两组之间无差异。结论潜阳通络方的降血压和逆转左室肥厚机制,初步认为与其降低体内CA的含量相关。     

Electrocardiographic diagnosis of exercise-induced left ventricular hypertrophy

To assess the prevalence of physiologic left ventricular hypertrophy and the usefulness of ECG criteria for its diagnosis, we compared ECGs and M-mode echocardiograms from 44 ultraendurance athletes and 20 similarly aged sedentary control subjects. Left ventricular mass was elevated in 25 of 44 (57%) athletes including 17 of 29 (59%) men greater than 134 gm/m2 and 8 of 15 (53%) women greater than 110 gm/m2. The sensitivity and specificity of the three ECG criteria used to diagnose left ventricular hypertrophy were: Sokolow-Lyon voltage (S-V1 + R-V5 greater than or equal to 3.5 mV), 65% and 61%; Romhilt-Estes score (greater than or equal to 4), 16% and 84%; and Cornell voltage (R-aVL + S-V3 greater than 2.8 mV in men and greater than 2.0 mV in women), 8% and 95%, respectively. Left ventricular mass, mass index, posterior wall thickness, chamber diameter, and relative wall thickness were not related to any measurement of QRS voltage. Nonvoltage ECG criteria for left ventricular hypertrophy were rare in athletes. Thus hypertrophy is a common but not universal adaptation to exercise. It is only moderately well detected by standard voltage criteria for left ventricular hypertrophy and is not reflected in nonvoltage criteria.