氯通道阻滞剂尼氟灭酸对肥厚心肌心室有效不应期及心室颤动阈值的疗效

背景 肥厚心肌离子通道的重塑容易发生恶性室性心律失常,钙激活氯通道的改变起着重要的作用,尼氟灭酸(NFA)是常用的钙激活氯通道的阻滞剂.目的 不同剂量NFA对左室肥厚心肌心室有效不应期及心室颤动阈值的影响.方法 32只10周龄雄性自发性高血压大鼠(SHR)随机分成非NFA处理组及3个NFA不同剂量(0.01,0.1,1.0 μmol/kg.iv)处理组,每组8只,取8只雄性Wistar大鼠作为对照组,分别测定各组大鼠心率、动脉收缩压、心室有效不应期、心室颤动阈值及左室质量指数.结果 1)SHR左室质量指数明显大于Wistar大鼠(P＜0.01);2)NFA非处理组的心室颤动阈值明显小于对照组[(15.0±1.2)mA vs(26.4±1.5)mA,P＜0.01);3)NFA浓度越大延长左室肥厚心肌的心室有效不应期越明显,提高左室肥厚心肌的心室颤动阈值越明显(P＜0.05),呈浓度依赖趋势;4)心室有效不应期与心室颤动阈值正相关,NFA的3个不同处理剂量与心室有效不应期或心室颤动阈值正相关.结论 NFA可以延长左室肥厚心肌的心室有效不应期,提高左室肥厚心肌的心室颤动阈值.     

异莲心碱防止高血压大鼠左室肥厚的可能机制

背景既往报告异莲心碱是从莲子心中分离的一种双苄基喹啉生物碱单体，具有抗心律失常、Ca^2＋拮抗及阻断α受体作用，对高血压左室肥厚有不同程度的改善。高血压左室肥厚心肌肌浆网钙泵（SERCA）活力较正常心肌降低。目的探讨异莲心碱对高血压大鼠左室肥厚及SERCA活力的影响。方法将二肾一夹肾血管性高血压大鼠（RHR）模型，随机分为3组：正常对照组、肾血管性高血压大鼠对照组（未治疗RHR组）和异莲心碱治疗组。在异莲心碱治疗组持续给药10周后，分别测定各组大鼠的血压、左室质量／体质量，以及左室心肌SERCA活力。结果治疗后，异莲心碱治疗组血压（136．4±14．6）mmHg较未治疗RHR组（189．8±4．4）mmHg显著降低（P〈0．01）；异莲心碱治疗组左室质量／体质量（2．23±0．43）也较未治疗RHR组（2．93±0．52）显著降低（P〈0．05）；异莲心碱治疗组左室心肌SERCA活力[（0．91±0．18）μmol／（gprotein·min）]较未治疗RHR组[（0．61±0．23）μmol／（gprotein·min）]显著升高（P〈0．05），但仍较正常对照组[（1．32±0．18）μmol／（gprotein·min）]低（P〈0．01）。结论异莲心碱能降低RHR的血压，减低RHR的左室质量／体质量，对高血压左室肥厚具有一定的防治作用；其机制可能与异莲心碱能升高RHR肥厚心肌肌浆网SERCA活力，改善心肌细胞内钙超载有关。     

缬沙坦对自发高血压大鼠左室心肌心室有效不应期和心室颤动阈值的影响

目的探讨缬沙坦对自发高血压大鼠左室心肌有效不应期和心室颤动(简称室颤)阈值的影响。方法16只10周龄雄性自发高血压大鼠随机分成缬沙坦组和非缬沙坦组,每组8只;8只10周龄Wistar大鼠做为对照组。喂药8周后分别测定各组大鼠动脉收缩压、左室质量指数、心室有效不应期和室颤阈值。结果①非缬沙坦组和缬沙坦组左室质量指数明显大于对照组(3.7±0.02 mg/g,3.2±0.03 mg/g vs 2.5±0.03 mg/g,P<0.001);非缬沙坦组左室质量指数明显大于缬沙坦组(P<0.001);②非缬沙坦组和缬沙坦组室颤阈值明显低于对照组(15.4±0.4 mA,18.6±0.5 mA vs 26.3±0.5 mA,P<0.001);缬沙坦组室颤阈值明显大于非缬沙坦组(P<0.001)。结论缬沙坦通过逆转自发高血压大鼠左室心肌肥厚提高左室心肌室颤阈值。     

Toll样受体在Goldblatt鼠左室心肌中的表达-炎症与左心室肥厚相关的一个证据

目的 观察肾血管性高血压大鼠（2K1C，Goldblatt高血压大鼠）左室心肌中Toll样受体4（Toll-like receptor4，TLR4）、核因子κB（NFκB）的表达情况并探讨其影响因素。方法 采用免疫组化法检测10只雄性Goldblatt高血压大鼠和6只正常雄性Sprague-Dawley（SD）大鼠左室心肌中TLR4、核因子κB的表达情况，维多利亚蓝一丽春红法行心肌胶原染色评价心肌纤维化程度，根据超声心动图评价左室结构和功能。结果 高血压大鼠左室心肌组织中TLR4和NFκB的表达水平升高（P〈0．01），两者呈高度正相关（r=0．824，P〈0．01）；TLR4表达水平与左室心肌纤维化呈正相关；TLR4表达水平与左室心肌肥厚程度、收缩功能指数显著相关。结论 TLR4信号通路的活化可能参与Goldblatt大鼠心肌肥厚的发生和发展。     

C型利钠肽在高血压病患者中的变化及其临床意义

目的 探讨原发性高血压患者C型利钠肽（CNP）的变化及临床意义。方法 用酶联免疫吸附法测定58例高血压病无左室肥厚组、50例高血压病伴左室肥厚组，及50例血压正常的健康成人对照组血清CNP浓度，采用多普勒超声心动图检查计算左室重量指数。结果 高血压病伴左室肥厚组CNP水平明显高于高血压病无左室肥厚及健康对照组，结果有显著差异（P〈0．01），高血压病无左室肥厚组高于健康对照组（P〈0．01）。CNP浓度与左室重量指数呈正相关（r-0．62，P〈0．01）。原发性高血压患者中伴心脑肾并发症组血清CNP浓度明显高于无并发症组（P〈0．01）。结论 CNP水平可以反映高血压及左室肥厚程度，CNP变化与病情严重程度相关。     

普伐他汀对胰岛素抵抗Wistar大鼠左室重量的影响

目的：探讨普伐他汀对高蔗糖饲料喂养诱导的胰岛素抵抗Wistar大鼠左室重量的影响及其可能机制。方法：雄性Wistar大鼠被分成3组：（1）胰岛素抵抗组（IR组,10只）：高蔗糖饲料喂养12周;（2）普伐他汀组（P组,10只）：高蔗糖饲料喂养12周,后4周每只每天加普伐他汀smg／kg灌喂;（3）正常对照组（5只）：普通饲料喂养12周。12周后量血压、断尾留取血标本检测血糖、血脂、血清胰岛素水平;处死动物,留取心肌标本检测左室相对重量（LVRW）、心肌内皮素（ET）和血管紧张素Ⅱ（AngⅡ）水平。结果：与对照组比较,IR组大鼠LVRW、心肌ET和AngⅡ水平明显升高,而胰岛素敏感指数（ISI）则明显降低（P均〈0．01）;体重和血压差异没有显著性（P〉0．05）。普伐他汀干预后的Wistar大鼠除了血压、心肌AngⅡ水平无显著差异外,心肌ET水平,LVRW均较IR组明显减少．胰岛素敏感指数（ISI）则明显回升（P〈0．01）。结论：普伐他汀可改善胰岛素抵抗Wistar大鼠的左室肥厚．其机制可能与改善胰岛索抵抗及减少局部心肌ET水平有关。     

腺病毒介导的心肌蛋白激酶Cε基因转移导致心功能损害

目的本文旨在研究腺病毒介导的成年小鼠心肌直接PKCε基因转移对左室收缩功能的影响。方法使用标准方法建立表达PKCt基因的重组腺病毒载体。直接注射重组腺病毒到FVB／N和ICR小鼠心肌，对照鼠给予相同剂量空载腺病毒。Western免疫印迹测定PKCε蛋白质表达水平。用非开胸经颈总动脉插管的显微外科技术评价小鼠左室收缩功能。结果与对照鼠相比基因转移鼠心肌转基因PKCε蛋白质表达水平增加近4倍，基线左室最大收缩压、最大收缩速率（dP／dt）、-dP／dt明显降低，左室舒张末压、舒张压明显升高（P〈0．01），异丙肾上腺素激发后左室dP／dt剂量依赖的升高明显减弱（P〈0．01），PKCε基因转移鼠心脏／体重比也较对照鼠明显增加（P〈0．01）。结论腺病毒介导的、心肌直接的PKCε基因转移诱发了左室收缩功能的损害，导致了心肌肥厚和心衰。     

原发性高血压合并左室肥厚患者的心率振荡

424例高血压患者，按照心脏彩色超声检查结果，将受试者分为左室肥厚组及左室正常组。全部受试者均接受24h长程心电图记录，计算震荡初始（TO）和震荡斜率（TS）。结果：与左室正常组比较，左室肥厚组TO增大，TS减小（P〈0．01）。左室肥厚组异常TO及TS发生率较左室正常组高（P〈0．01）。结论：高血压伴左室肥厚患者的HRT明显减弱，提示高血压合并左室肥厚时，自主神经功能受损加重。     

伊贝沙坦对高血压左室肥厚患者的左室结构的影响

目的 研究伊贝沙坦对高血压左室肥厚（LVH）患者的左室结构的影响。方法 60例原发性高血压左室肥厚患者随机分为2组：治疗组每天口服伊贝沙坦150mg，对照组每天口服氨氯地平5mg。平均12个月，观察用药后血压、左室结构的变化。结果 用药后2组收缩压（SBP）和舒张压（DBP）均显著降低（P〈0．01）；室间隔厚度（IVST）及左室后壁厚度（LYPWT）均变薄（P〈0．01），左室重量指数（LYMI）明显减少（P〈0．01），对照组各项指标无明显变化（P〈0．05）。结论 对原发性高血压左室肥厚的患者，长期应用伊贝沙坦具有良好降压效果，同时还可逆转LVH，改善患者预后。     

血浆内皮素和降钙素基因相关肽与高血压左室肥厚的关系研究

目的检测高血压左室肥厚（LVH）患者血浆内皮素和降钙素基因相关肽的浓度，期望进一步揭示高血压左室肥厚的发病机制。方法选择健康成年人30名为正常对照组，严格按照2005年《中国高血压防治指南》标准选取1、2级原发性高血压（EH）患者90例，其中非左室肥厚组30例，左室肥厚组60例，测量血压、左室室间隔厚度（IVST）、左室后壁厚度（PWT）及采取肘静脉血3ml，分离血浆，测量血浆内皮素和降钙素基因相关肽的浓度。所得数据用x±s表示，采用t检验和直线相关检验。结果①高血压组血浆内皮素的浓度均高于正常对照组（P〈0．01），左室肥厚组高于非左室肥厚组（P〈0．05），左室肥厚组左室室间隔厚度、左室后壁厚度与血浆内皮素的浓度呈正相关。②高血压组患者血浆降钙素基因相关肽的浓度均低于正常对照组（P〈0．01），左室肥厚组低于非左室肥厚组（P〈0．01），左室肥厚组左室室间隔厚度、左室后壁厚度与血浆降钙素基因相关肽的浓度呈负相关。③内皮素／降钙素基因相关肽比值在正常对照组接近于1，在高血压组大于1，其中左室肥厚组大于非左室肥厚组。结论血浆内皮素、降钙素基因相关肽的浓度比例失衡参与了高血压及左室肥厚的发生，二者在高血压及左室肥厚的发生、发展中具有不可忽视的作用，所以通过检测血浆内皮素、降钙素基因相关肽的浓度可能对高血压的诊断及临床治疗评价都起着重要作用。     

Mechanisms of Arrhythmias in Ventricular Hypertrophy

Mechanisms of Arrhythmias in Ventricular Hypertrophy. Cardiac hypertrophy is an adaptative process by which the heart accommodates to abnormal pressure and volume overloads. However, hypertrophy of the left ventricle is associated with a high incidence of ventricular arrhythmias and sudden death. The cellular mechanisms responsible for the abnormal rhythmic activity in hypertrophied myocardium has not been clearly defined, but left ventricular hypertrophy is associated with characteristic electrical abnormalities in experimental models and in hypertrophied human tissue. The most consistent electrical alteration is prolonged duration of the action potential in hypertrophied myocardium. The prolonged duration of depolarization predisposes hypertrophied tissue to develop early afterdepolarizations, which can encourage the development of arrhythmias by a variety of mechanisms. Early afterdepolarizations interrupt repolarization and can lead directly to sustained triggered activity. Early afterdepolarizations can depolarize adjacent excitable fibers and thereby induce triggered activity. The prolonged duration of repolarization can enhance influx of calcium, which can in turn lead to delayed afterdepolarizations that can give rise to triggered activity. Early afterdepolarizations can also produce conduction block or delay, which could contribute to the development of reentrant arrhythmias. Early afterdepolarizations are the most likely electrical abnormality to arise from the prolonged time course of repolarization in hypertrophied myocardium. Therefore, therapeutic measures aimed at preventing the development of early afterdepolarizations in hypertrophied myocardium could prove to be a fruitful approach to inhibiting the development of arrhythmias. The development of agents that selectively reduce the duration of the action potential requires a better understanding of the ionic mechanisms responsible for prolonging the action potential in hypertrophied myocardium. In the meantime, avoiding factors known to favor the development of afterpotentials (e.g., extremes of heart rate, electrolyte abnormalities, certain antiarrhythmic drugs) in patients with left ventricular hypertrophy seems prudent.     

卡维地洛对压力负荷性大鼠心室重构及ET-1 mRNA表达的影响

目的　研究第三代 β受体阻滞剂卡维地洛对压力负荷性大鼠心室重构及心肌ET 1mRNA表达的影响。 方法　 2 0只Wistar大鼠行腹主动脉缩窄术造成后负荷增高型大鼠模型 ,随机分为肥厚组和卡维地洛组 ,4周药物干预后测定血流动力学指标和心室重量指数 ,心肌ET 1mRNA的表达水平。结果　肥厚组MBP和LVSP升高 (P <0 0 5 ) ,LVMI和RVMI升高 18 1% ,2 7 7% (P <0 0 5 ) ,ET 1mRNA表达增加 2 0 9% (P <0 0 1) ;卡维地洛改善血液动力学指标 (P <0 0 1～0 0 5 ) ,降低LVMI和RVMI(P <0 0 5 ) ,下调心肌ET 1mRNA的表达 (P <0 0 5 )。结论　压力负荷性大鼠表达上调的ET 1参与心室重构。卡维地洛下调ET 1的过度表达可能是其防治心室重构的机制之一     

Dispersion of Ventricular Repolarization in Left Ventricular Hypertrophy: Influence of Afterload and Dofetilide

Modulators of APD Dispersion in Hypertrophy. Introduction: Increased dispersion of ventricular repolarization is observed in cardiac hypertrophy and is associated with sudden cardiac death. At present, there is little information about the effects of cardiac hemodynamics and antiarrhythmic drugs on dispersion of repolarization in disease states. We compared the effects of increasing afterload and the Class III antiarrhythmic drug, dofetilide, on dispersion of ventricular repolarization in hypertrophied rabbit hearts to normal rabbit hearts. Methods and Results: Cardiac hypertrophy was induced in rabbits by abdominal aortic banding. Isolated hearts were studied 49 ± 4 days postsurgery in the working heart mode using a blood-buffer perfusate. The action potential duration (APD) was measured from eight sites on the epicardium of the heart at low (50 ± 7 mmHg) afterload and high afterload (97 ± 12 mmHg) at baseline and during dofetilide perfusion. APD dispersion, determined as the difference between the maximal and minimal APD, was greater in hypertrophied hearts (42 ± 8 msec) compared with control hearts (26 ± 8 msec, P < 0.05) at baseline and low afterload. Increasing afterload caused a decrease in APD dispersion in hypertrophied hearts (P < 0.05) but not in control hearts, and APD dispersion was similar in hypertrophied hearts (31 ± 9 msec) compared with control hearts (30 ± 9 msec, P= NS). During dofetilide perfusion, APD dispersion remained greater in hypertrophied hearts (60 ± 39 msec) compared with control hearts (30 ± 13 msec, P < 0.05) at low afterload but not high afterload. Increasing afterload caused shortening of the APD in most regions of the control hearts, whereas APD did not shorten significantly in hypertrophied hearts at baseline and tended to increase during dofetilide perfusion. During dofetilide perfusion, the maximal change in APD recorded from the posterior wall of the left ventricle following an increase in afterload was ?18 ± 21 msec in control hearts and 7 ± 21 ms in hypertrophied hearts (P < 0.05). Conclusion: Epicardial APD dispersion decreases in hypertrophied hearts following an increase in afterload, and this response is mediated in part by the absence of afterload-induced shortening of the APD. This effect may be due in part to aftered responses of the delayed rectifying current to cardiac loading conditions in the setting of cardiac hypertrophy.     

Tricuspid Atresia with Absent Pulmonary Valve and Intact Ventricular Septum: A Rare Association

The absence of the pulmonary valve in connection with tricuspid atresia and intact ventricular septum is a rare malformation, associated with a poor prognosis. The right ventricle is severely hypertrophied, resembling a cardiac mass protruding into the left ventricular outflow tract. We report such a case that underwent successful palliation with a Blalock–Taussig shunt followed by a superior cavopulmonary anastomosis.     

Effect of Losartan on Right Ventricular Hypertrophy and Cardiac Angiotensin I-Converting Enzyme Activity in Pulmonary Hypertensive Rats

The aim of this study was to investigate the effect of prophylactic treatment with the angiotensin type 1 (AT₁) receptor antagonist losartan on right ventricularhypertrophy and cardiac angiotensin I-converting enzyme (ACE) activity in a rat model of monocrotaline-induced pulmonary hypertension. Losartan failed to prevent either pulmonary hypertension or right ventricular hypertrophy. Right ventricular ACE in untreated pulmonary hypertensive rats did not differ from control rats. Losartan treatment in pulmonary hypertensive rats caused a significant 2-fold increase of ACE activity in the hypertrophied right (p<0.005) but not in the left ventricle. Thus, cardiac ACE activity is not stimulated in rats with monocrotaline-induced right ventricular hypertrophy. Prophylactic losartan treatment in this model of progressive pulmonary hypertension failed to prevent or reduce the increase in ventricular afterload. The relevance of the increase in right ventricular ACE activity during pulmonary hypertension after losartan treatment is unknown and needs to be evaluated in further studies.     

Ventricular arrhythmias, increased cardiac calmodulin kinase II expression, and altered repolarization kinetics in ANP receptor deficient mice

Cardiac hypertrophy is associated with ventricular arrhythmias and sudden death. The molecular mechanisms that predispose the hypertrophied heart to arrhythmias are not well understood. In mice, deletion of the gene coding for the atrial natriuretic peptide receptor, guanylyl cyclase A (GC-A-/-), causes arterial hypertension, cardiac hypertrophy and sudden death. We used this mouse model to study molecular mechanisms of arrhythmias in the hypertrophied heart. Right and left ventricular monophasic action potential durations (APD) were recorded in isolated, Langendorff-perfused hearts during pacing from the right atrium and ventricle. The atrioventricular (AV) node was ablated to provoke bradycardia. Intracellular Ca(2+) transients were measured in isolated INDO-1 loaded ventricular myocytes. Cardiac expression of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) was analyzed by western blotting. Polymorphic ventricular arrhythmias (pVT) occurred spontaneously after mechanical AV block in 20/45 hearts from 12-month-old GC-A-/- mice (P < 0.05), but neither in age-matched GC-A+/+ hearts nor in hearts from 3-month-old mice of either genotype. Triggered activity preceded pVT. APD were prolonged and systolic Ca(i)(2+) levels were increased in GC-A-/- hearts independently of age. In 12-month-old GC-A-/- hearts only, dispersion of APD and expression levels of CaMKII were increased. CaMKII expression was particularly increased in hearts with pVT. Direct inhibition of CaMKII activation by KN93 (0.5 or 2 microM) or inhibition of Ca(2+)/calmodulin-dependent activation of CaMKII by W-7 (25 microM) suppressed pVT in GC-A-/- hearts (P < 0.05) while prolonging APD. The combination of increased CaMKII activity and altered action potential characteristics facilitates ventricular arrhythmias in hypertrophic GC-A-/- hearts.     

Susceptibility of hypertrophied rat hearts to ventricular fibrillation during acute ischemia

This study compared arrhythmias induced by acute ischemia in Langendorff preparations of normal and hypertrophied rat hearts. Left ventricular pressure overload was induced by partial ligation of the abdominal aorta 6 to 8 weeks prior to study. The ratio of left ventricular weight to body weight (LVW/BW) and systolic blood pressure (SBP) were significantly higher in two groups of rats with hypertrophied hearts (moderate hypertrophy: 2.68 +/- 0.06 mg/g, 182 +/- 3 mmHg; severe hypertrophy: 3.31 +/- 0.03 mg/g, 238 +/- 5 mmHg) than in normal hearts (2.18 +/- 0.03 mg/g, 125 +/- 3 mmHg), while there were no differences in body weights. During 30 min of ischemia produced by left coronary artery occlusion in the Langendorff preparations, ventricular fibrillation occurred in six of 20 (30%) normal, six of nine (67%) moderately hypertrophied, and 14 of 14 (100%) severely hypertrophied preparations (P less than 0.001 normal vs severely hypertrophied). Tachyarrhythmias occurred in 15 of 20 (75%) normal, eight of nine (89%) moderately hypertrophied, and 14 of 14 (100%) severely hypertrophied hearts. Heart rate and coronary efflux before and during the ischemic period did not differ between normal and hypertrophied hearts. The ratio of non-perfused to perfused areas of the left ventricle, measured by Evans blue dye staining and with computerized planimetry, also was not different for normal (57.6 +/- 2.3%) and hypertrophied hearts (moderate hypertrophy 62.5 +/- 3.3%, and severe hypertrophy 59.1 +/- 2.0%). Additional control studies using larger hearts from older rats also indicate that myocardial mass was not an important determinant of ischemic arrhythmias in hypertrophy. Prolongation of endocardial and epicardial conduction time during 30 min of ischemia was not different between normal and hypertrophied hearts. Action potential duration and refractory periods were significantly longer in ventricular cells of hypertrophied hearts than in normals, and superfusion with hypoxia/zero glucose solution shortened these parameters to a greater extent in hypertrophied cells. These results lead us to conclude that hypertrophied hearts have a greater susceptibility to ventricular fibrillation during acute ischemia, and that dispersion of refractoriness may play a role in this phenomenon.     

Association of Left Ventricular Diverticula and Sinus Venosus Atrial Septal Defect

Left ventricular diverticula are congenital anomalies and are not as rare as previously thought. In adults, cardiac diverticula are generally accidental findings during imaging modalities, but concomitant disorders might frequently coexist. The pathophysiology, management, prognosis, and natural history of cardiac diverticula remain poorly understood and controversial. Definite diagnosis is often challenging due to similarities in appearance to other more common anomalies such as aneurysms, pseudoaneurysms, endocarditis, cysts, and hypertrophied trabeculations. We herein report a rare case of an adolescent presenting with sinus venosus atrial septal defect, partial anomalous venous connection, and left ventricular diverticula.     

Relationship between the high-energy phosphate content and various left ventricular functional parameters of the normal and hypertrophied heart after global ischemia and reperfusion

Using an isolated rat heart preparation (Langendorff perfusion, perfusion pressure 100 cm H2O) the correlation between the high-energy phosphate content and various left ventricular (lv) functional parameters of the hypertrophied heart (spontaneous hypertensive rats lv/body weight ratio 3.6 +/- 0.5 x 10(-3) was determined after normo- (30 min) and hypothermic (25 degrees C, 120 min) cardioplegic arrest and reperfusion, and compared with normal hearts (Wistar rats lv/body weight ratio 2.0 +/- 0.3 x 10(-3). St. Thomas Hospital solution was used as the cardioplegic agent. Before ischemia hypertrophied hearts had a significantly higher developed left ventricular pressure, pressure rate product and dp/dtmax, but a significantly lower ATP and total adenine nucleotide content. Irrespective of the mode and temperature of cardiac arrest there was a strong correlation both for normal and for hypertrophied hearts between the high-energy phosphate content expressed as ATP, total adenine nucleotides or the "energy charge" and the left ventricular functional parameters pressure rate product and dp/dtmax. The correlation coefficient ranged from 0.80 to 0.89 and was highest when the ATP content was plotted against pressure rate product (r = 0.89). There was a different slope for normal and hypertrophied hearts with a steeper decline of the left ventricular function in hypertrophied hearts for any given reduction of the myocardial adenine nucleotide content. Our results indicate that a similar reduction of the ATP or total adenine nucleotide content in both the normal and hypertrophied heart reduces left ventricular function to a greater degree in the hypertrophied heart.