The usefulness of the electrocardiogram in the diagnosis of left ventricular hypertrophy in essential arterial hypertension]

The aim of the study is to analyse the usefulness of electrocardiographic criteria of left ventricular hypertrophy in essential hypertension. Seventy four patients (27 males, 47 females), 49 +/- 11 years--old with mild--moderate systemic hypertension (blood pressure greater than or equal to 140/90 mmHg) have been prospectively studied. A 12-lead electrocardiogram and an echocardiogram (M and 2D mode) have been performed after the basic clinical study. A left ventricular mass index (Devereux's method) greater than 131 g/square meters (males) or greater than 110 g/square meters (females) has been considered as left ventricular hypertrophy. Sensitivity, specificity and accuracy of 11 current electrocardiographic criteria of left ventricular hypertrophy have been determined. Sensitivity of these criteria was very low (0-0.35), while specificity was high (0.71-1). Total QRS voltage showed the best accuracy (0.51), while V5 or V6 R wave amplitude greater than 26 mm showed the best sensitivity (0.35). Current electrocardiographic criteria of left ventricular hypertrophy are not very useful in the diagnosis of left ventricular hypertrophy in essential hypertension.     

Prediction of left ventricular ejection fraction using a unique method of chest x-ray and ECG analysis: a noninvasive index of cardiac performance based on the concept of heart volume and mass interrelationship

A reasonably accurate, simple, inexpensive, noninvasive method of determining ejection fraction (EF) is necessary to evaluate left ventricular function in epidemiologic studies and individual patients. Using the concepts of left ventricular mass reflected by precordial R wave summation (M) and left ventricular volume (V) estimated by chest roentgenography in 114 patients with myocardial disease undergoing left ventriculography, EF was predicted with the formula: EF = 63.74 - (2.16.V) + (0.34.M); R2 = 0.69; standard error of the estimate (SEE) = 11. Because angiographic inferior wall motion (IWM) abnormalities significantly affected the results, but inferior Q waves were usually only present in patients having one infarct, a noninvasive technique to predict the presence of inferior wall motion abnormality (IMA) in patients having multiple infarcts was developed and based on the relationship of precordial R wave summation (M) and roentgenographic heart volumenometry (V). By combining V, M, and IMA (which predicted IWM) to determine EF, multiple linear regression analysis showed that EF = 67.30 - (1.56.V) + (0.23.M) - (14.18 IMA) (R2 = 0.77; SEE = 9). Prospective validation of the formula was then done in 139 consecutive individuals, with R2 = 0.49 and SEE = 9. This study demonstrates that routinely performed, simple, inexpensive clinical tests provide data that can be combined by multiple regression analysis to predict resting EF in patients with heart disease affecting the left ventricle. This unique method may allow inexpensive ventricular function screening in large population studies and in addition might provide an independent index of myocardial performance for clinical use, since it reflects the amount of contractile mass per unit of left ventricular volume.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac contractile proteins in hypertrophied and failing guinea pig heart.

OBJECTIVE: The aim was to study changes in contractile proteins which accompany marked hypertrophy and heart failure in mammalian hearts initially containing predominantly V3 isomyosin. METHODS: Left ventricular myosin and myofibrillar ATPase activity and right ventricular actomyosin ATPase activity were measured in normal guinea pig hearts, in hearts which were hypertrophied as a result of progressive left ventricular systolic overload following ascending aortic banding, and in hypertrophied hearts from animals which showed signs of overt congestive heart failure. Male guinea pigs weighing 225-275 g at the time of aortic banding were used for the studies. RESULTS: Left ventricular myosin and myofibrillar ATPase activity and right ventricular actomyosin ATPase activity were correlated with body weight, left and right ventricular weight, and left ventricular peak systolic pressure during aortic occlusion. Left ventricular myosin ATPase activity and right ventricular actomyosin ATPase activity were markedly depressed in hypertrophied ventricles compared to control ventricles. Cardiac myofibrillar ATPase activity was lower in hypertrophied failing hearts than in control hearts over a wide range of calcium concentrations. In control animals and in those without heart failure, there was a nearly identical inverse relationship between left ventricular mass up to 1600 mg and myosin ATPase activity. Hypertrophied failing hearts were larger but showed little further reduction in cardiac myosin ATPase activity. Representative gel scans of non-dissociating pyrophosphate gels of left ventricular myosin from an 8 d postoperative aortic constricted animal and from its age and weight matched control showed predominantly V3 isomyosin with small amounts of V1 isoenzyme. However, preparations taken from guinea pigs 16 d after aortic constriction showed only the V3 isoform, whereas the V1 isoform was still apparent in control. Hypertrophied failing left ventricles developed less pressure per unit mass during brief aortic occlusion than non-failing left ventricles with comparable myosin ATPase activities. CONCLUSIONS: These observations raise important questions as to the distribution of myosin isoforms in the normal adult guinea pig, and the possibility that myosin ATPase activity might be altered by post-translational modification. Although cardiac myosin ATPase activity correlates with left ventricular performance, it cannot fully explain the depressed performance of failing hearts in this model. Additional immunological studies of cardiac contractile proteins are required as well as studies designed to explore the implications of altered myosin ATPase activity for both contractile function and overall cellular homeostasis.     

Electrocardiographic detection of left ventricular hypertrophy: development and prospective validation of improved criteria

To develop improved electrocardiographic criteria of left ventricular hypertrophy, individual electrocardiographic voltage measurements were compared with echocardiographic left ventricular mass in a "learning series" of 414 subjects. The strongest independent relations with left ventricular mass were exhibited by the S wave in lead V3, the R wave in lead a VL and the T wave in lead V1 (each p less than 0.001), and by age and sex. Better electrocardiographic detection of left ventricular hypertrophy was achieved by new criteria that stratified QRS voltage and repolarization findings in sex and age subsets. For men, at all ages, left ventricular hypertrophy is suggested by QRS voltage alone when the R wave in lead aVL and the S wave in lead V3 total more than 35 mm. When this voltage exceeds 22 mm, left ventricular hypertrophy is suggested in men under age 40 years when the T wave in lead V1 is positive (greater than or equal to 0 mm), and in men 40 years or older when the T wave in lead V1 is at least 2 mm. For women, at all ages, left ventricular hypertrophy is suggested when the R wave in lead a VL and the S wave in lead V3 total more than 25 mm. When this voltage exceeds 12 mm, left ventricular hypertrophy is suggested in women under 40 when the T wave in lead V1 is positive (greater than or equal to 0 mm), and in women over 40 when the T wave in lead V1 is 2 mm or greater.(ABSTRACT TRUNCATED AT 250 WORDS)     

Subarachnoid hemorrhage complicated with different manifestations of transient abnormal left ventricular wall motion: two case reports

Two patients with subarachnoid hemorrhage presented with transient abnormal left ventricular wall motion. Case 1 was a 56-year-old man. Electrocardiography showed ST segment elevation in leads I, II, II, aVL, aVF, V3-V6. Echocardiography showed localized left ventricular hypokinesis around the apical area (takotsubo-like cardiomyopathy). Ejection fraction was 20% (1st hospital day). Troponin T was positive. Case 2 was a 48-year-old woman. Electrocardiography showed ST segment elevation in leads I, aVL, V2-V6 and ST segment depression in leads II, III, aVF, V1. Echocardiography showed diffuse left ventricular hypokinesis. Ejection fraction was 21% (1st hospital day). Troponin T was positive. These two patients had no history of cardiac disease, and coronary angiography showed no stenosis or obstruction. Catecholamine was given for 1 day(Case 1) and for about 2 weeks (Case 2). Pimobendane was given to Case 2. Ejection fraction was 57% in Case 1 (2nd hospital day) and 33% (6th hospital day), 43% (7th hospital day)and 58% (16th hospital day)in Case 2. The recovery period of left ventricular abnormal wall motion and the medication period were longer in Case 2 showing diffuse hypokinesis than in Case 1 showing takotsubo-like cardiomyopathy.     

Electrocardiogram in dilated cardiomyopathy

The authors describe the main electrocardiographic features in 90 cases of dilated cardiomyopathy. The patients were divided into tree groups: in group I were the patients with electrocardiographic signs of left ventricular hypertrophy, in group II the patients with complete left bundle branch block and in group III the cases with right bundle branch block, was held in the group I 64 patients (71%), in the group II 22 (24.6%) and in the group III four case (4.4%). Seventy two cases (80%) showed arrhythmias. Atrial fibrillation was observed in 20 patients (28%), supraventricular tachycardia in two (3%), atrioventricular block, of the 1st and 2nd degree, in eight (11%), ventricular arrhythmias in 63 (87.5%) and supraventricular arrhythmias in 42 (58%). In the 64 patients, with left ventricular hypertrophy, 60 (93.75%) showed very important S waves in, at least two right precordial leads. Fourty four patients (73.3%) had rS pattern in right precordial leads, from V1 to V4, with the R waves in V5 and V6 with normal, low and height amplitude. A first degree left bundle branch block was recorded in 16 cases (25%), a pathologic Q waves in 22 (37.5%), low voltage in limb leads in 24 (37.5%), left atrial enlargement in 36 (56%), right atrial enlargement in two (3%) and atrial fibrillation in 10 (16%). In the 22 patients from the group II six (27%) had left atrial enlargement, two (9%) had right atrial enlargement and six (27%) atrial fibrillation. In the four patients from group III two (50%) had an incomplete right bundle branch block, two (50%) the complete form and all had atrial fibrillation.     

左束支阻滞型特发性室性心动过速的心电图特征对射频消融成功的影响初探

对心电图呈左束支阻滞型的特发性室性心动过速 (简称室速 )的临床特点和心电图进行分析 ,以了解哪些因素可以预测此类患者从右室流出道行射频消融的成功率。对 2 6例特发性室速的患者进行电生理检查和射频消融手术 ,全部患者室速时的心电图呈左束支阻滞。结果 :2 6例中 ,2 2例于右室流出道进行了成功消融 ,成功和未成功消融的患者临床特征和电生理无明显区别 ,成功消融的患者中胸前V1 导联心电图呈rS型 (1 2例 )和QS型 (1 0例 ) ,而 4例未成功者 ,V1 导联均呈rS型 ,其中 2例经主动脉于左冠状窦消融成功。在成功与未成功消融患者中 ,V1 导联有无R波无明显区别 ,但V1 导联无R波预示室速可以从右室流出道成功消融 ,成功消融的室速患者胸前导联的平均移行区在V4导联 ,而未成功患者胸前导联的移行区在V3 或V2 导联。结论 :某些心电图呈左束支阻滞 ,且额面电轴正常或右偏的特发性室速患者不能成功从右室流出道消融 ,V1 导联有r波且移行区在V3 导联或之前者提示此类心电图特征的室速可能非起源于右室流出道 ,部分可能起源于左室流出道     

Tako-tsubo cardiomyopathy: is there a preferred time of onset?

The occurrence of major cardiovascular events is not randomly distributed over time, but exhibits chronobiological patterns, i.e., circadian, weekly, or seasonal. No systematic studies on the temporal preference of onset of Tako-tsubo cardiomyopathy (TTC) are known. We performed a computer-assisted search of the literature (from 2000 to January 2010), with the following search terms: transient left ventricular apical ballooning syndrome, takotsubo-like left ventricular dysfunction, ampulla cardiomyopathy, tako-tsubo or takotsubo cardiomyopathy, tako-tsubo, apical ballooning. Criteria for publication inclusion were (a) reporting of original data, (b) inclusion of at least 30 or more cases, (c) adherence to the requested diagnostic criteria for TTC. We focused on studies including in their purposes the “time of onset” of events. Out of the 19 studies found, 7 (4 from Europe, 1 each from Asia, Australia and USA) specifically addressed this aspect. A circadian (morning) and a seasonal (summer) higher frequency of events was found. TTC seems to exhibit a temporal variation of onset, with preferred peaks during morning and summer. Stress and catecholamines, also according to their temporal organization, might play a pivotal role. The demonstration of time frames characterized by highest frequency of occurrence might help to try to ensure maximal protection during particularly vulnerable periods.     

P-wave configuration as an indicator of echocardiographic indices of cardiac structure and function in normotensive adolescents

We evaluated the associations of a bimodal P-wave in ECG lead V1 to cardiac structure and function in healthy normotensive adolescents. Two-dimensional-guided M-mode echocardiography, 12-lead ECG, and conventional and 2-hour averaged automated blood pressure (BP) measurements were obtained in 40 normotensive (conventional BP less than 140/90 mm Hg) adolescents (mean age, 13 +/- 1 years). Compared with subjects with simple unimodal P-waves (n = 18), those with a normal yet bimodal P-wave in lead V1 (n = 22) had higher two-hour averaged systolic BP (108 +/- 12 mm Hg vs 99 +/- 7 mm Hg, p less than 0.01) and conventional sphygmomanometer systolic BP (110 +/- 11 mm Hg vs 103 +/- 10 mm Hg, p = 0.05). Structurally, the bimodal P-wave group had greater left ventricular mass (174 +/- 40 g vs 144 +/- 26 g, p less than 0.01), and functionally, they had a greater stroke volume (68 +/- 15 ml vs 57 +/- 13 ml, p less than 0.05) than the unimodal P-wave group. In the group with bimodal P-waves, left atrial size was directly related to left ventricular mass (r = 0.63). By step-wise multiple linear regression analysis, this correlation coefficient increased to 0.74 with inclusion of heart rate and to 0.82 with inclusion of systolic BP. Although left atrial size was similar in the unimodal and bimodal P-wave groups, it was unrelated to any parameter in the unimodal P-wave group. Thus, a bimodal P-wave in lead V1, while generally considered a normal variant, is associated with slightly higher systolic BP, significantly greater left ventricular mass, and greater stroke volume. Additionally, a bimodal P-wave in V1 is predictive of the parameters that influence left atrial size, especially left ventricular mass. While all of these findings fall within the traditionally defined normal ranges, the existence of a bimodal P-wave might identify young individuals who are vulnerable to early cardiovascular manifestations of hypertension.     

Two cases of bi-ventricular dysplasia associated with ventricular tachycardia and familial occurrence of sudden death.

Two strikingly similar patients with arrhythmogenic right ventricular dysplasia which severely impaired not only the right ventricle but also the left ventricle are described in association with familial occurrence of sudden death. A 49-year-old man experienced syncope which was due to ventricular tachycardia. Electrocardiography revealed a first degree atrioventricular block, incomplete right bundle-branch block, T wave inversions in leads II, III, a VF and V1 to V5, and multiformal ventricular extrasystoles. Echocardiography and ventricular cineangiography showed not only the right ventricular dilatation with an aneurysm in the right ventricular apex, inflow and outflow tracts, but also mild dilatation of the left ventricle with left ventricular apical and posterior aneurysms. Radionuclide angiography also disclosed dysfunction of both ventricles, especially during exercise. His family history revealed that 3 members of his family died of sudden deaths. A 56-year-old woman experienced syncope secondary to ventricular tachycardia, with left bundle-branch block. Electrocardiography showed complete right bundle-branch block, left axis deviation, and T wave inversions in leads V1 to V4. Echocardiography and ventricular cineangiography revealed not only marked right ventricular dilatation with the "triangle of dysplasia", but also a left ventricular aneurysm in the apex and posterior portion. Her elder brother died of a sudden death, and electrocardiograms of 2 members of her family showed ventricular extrasystoles and T wave inversions. These 2 cases may well be termed "familial bi-ventricular dysplasia".     

Clinical implication of left precordial T wave inversions in the presence of complete right bundle branch block

This study was designed to elucidate whether left precordial negative T waves are electrocardiographic indicators for the diagnosis of hypertrophic cardiomyopathy (HCM) even in the presence of complete right bundle branch block (CRBBB). In 7 consecutive patients with CRBBB accompanied by negative T waves in at least one of the left precordial leads (V4, V5, V6, maximal negativity; 1.06 +/- 0.40 mVol) (left precordial negative T wave group) and in 15 randomly selected CRBBB patients without left precordial T wave inversions (control group), echocardiography was performed to rule out underlying diseases causing left ventricular overload and to identify candidates for magnetic resonance (MR) imaging. None had anginal pain indicating ischemic heart disease. When 2-dimensional echocardiography indicated left ventricular hypertrophy with wall thickness > or = 15 mm, the magnitude and distribution of hypertrophy were scrutinized on contiguous left ventricular MR short-axis images. The diagnostic criterion of HCM was the demonstration of hypertrophy with a wall thickness of 20 mm or more on the left ventricular MR short-axis images. All patients in the left precordial negative T wave group had negative T waves in both I (negativity; 0.27 +/- 0.17 mVol) and aVL (negativity; 0.23 +/- 0.14 mVol), whereas none in the control group did. The diagnostic criterion for HCM was fulfilled in six patients in the left precordial negative T wave group. However there were no patients who fulfilled the criterion in the control group. Negative T waves were recorded in the I (negativity; 0.30 +/- 0.17 mVol), aVL (negativity; 0.25 +/- 0.14 mVol), V4 (negativity; 1.03 +/- 0.46 mVol), V5 (negativity; 0.83 +/- 0.37 mVol) and V6 leads (negativity; 0.31 +/- 0.31 mVol) in all patients with HCM, while they were recorded in only 6% of the patients without HCM. In conclusion, the existence of left precordial negative T waves in the presence of CRBBB strongly indicates HCM.     

Left ventricular peak systolic pressure/end-systolic volume ratio change after dobutamine infusion for predicting left ventricular contractile reserve: comparison with Emax

OBJECTIVES: Genuine left ventricular contractile function is difficult to assess in the clinical setting. Left ventricular peak systolic pressure/end-systolic volume (Pps/Ves) ratio may be misleading because this index takes no account of the left ventricular end-systolic point and V0 intercept in the pressure-volume relation geographic curve. End-systolic pressure-volume relation and maximum chamber elastance derived from left ventricular pressure-volume loops can provide reliable estimates of contractile function. However, the feasibility of this technique for clinical purposes is limited, because it requires instantaneous measurement of left ventricular pressure and volume. This study assessed the feasibility of using Pps/Ves ratio for predicting the left ventricular contractile reserve by direct comparison with maximum elastance (Emax) derived from left ventricular pressure-volume loops. METHODS: Studies were undertaken in 18 consecutive patients aged 60 +/- 9 years who underwent cardiac catheterization. On-line instantaneous left ventricular volume was derived from the acoustic quantification method by transthoracic echocardiography. Pps was determined by pressure manometer tipped wire and Ves was measured automatically from acoustic quantification software in an ultrasound system. Pps/Ves was compared with Emax derived from each simultaneous pressure-volume loop during inferior vena caval occlusion before and after dobutamine infusion. Emax was determined as the slope of end-systolic points for each loop with the use of an automated iterative linear regression technique. Left ventricular contractile reserve was assessed by evaluating its functional response to 10 micrograms/kg/min of dobutamine infusion. RESULTS: Pps/Ves showed significant correlation with Emax in all patients (r = 0.70, p < 0.0001). However, scattered distribution of V0 value differences were noted. Contractile reserve (Pps/Ves) showed strong correlation with contractile reserve (Emax) despite V0 value differences (r = 0.927, p < 0.0001). CONCLUSIONS: Pps/Ves change after dobutamine infusion may minimize individual V0 distribution. This simple index could be used to evaluate left ventricular systolic performance without requiring the left ventricular pressure-volume relationship and volume unloading maneuver.     

Improvement of left ventricular wall synchronization with multisite ventricular pacing in heart failure: a prospective study using Doppler tissue imaging

We sought to assess right, left and biventricular pacing effects on myocardial function by using pulsed-Doppler tissue imaging (DTI) and automated border detection (ABD) techniques which provide electromechanical delay (EMD) assessment of the different left ventricular walls. METHODS: 15 patients (67+/-7 years) with drug-resistant primitive dilated cardiomyopathy and QRS> or =140 ms received a pacemaker for multisite ventricular pacing. Echocardiography was performed after 1 month of biventricular pacing (BVP). Echocardiographic measurements were recorded during spontaneous rhythm (SpR), right ventricular pacing (RVP), left ventricular pacing (LVP) and BVP. RESULTS: LV ejection fraction was statistically similar between the four rhythms. BVP showed a significant EMD decrease for the lateral LV wall vs. SpR, RVP and even LVP. LVP resulted in significantly longer aortic pre-ejection time vs. BVP while the EMD temporal dispersion (time between the shortest regional EMD and the longest one) was similar in the two modes. CONCLUSIONS: BVP and LVP substantially reduce the EMD temporal dispersion of the four LV walls, but with a longer aortic pre-ejection time for LVP. In RVP, LVP and BVP, the septal LV wall is always activated later than during SpR. BVP and LVP are associated with a mitral regurgitation reduction.     

Class I antiarrhythmic drug and coronary vasospasm-induced T wave alternans and ventricular tachyarrhythmia in a patient with Brugada syndrome and vasospastic angina

A 50-year-old man presented with a history of transient chest pain and palpitations. The 12-lead ECG at rest showed normal sinus rhythm. A slight ST segment elevation was observed in leads V1 to V3. During hospitalization, atrial fibrillation developed, and oral pilsicainide was administered. Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V1 to V3, and T wave alternans became visible in leads V2 and V3. Self-terminating ventricular tachycardia was initiated following frequent ventricular premature complexes, which showed a left bundle branch block pattern. The coronary angiogram was normal, but in the provocation test of vasospastic angina, acetylcholine administration into the left coronary artery resulted in complete occlusion of the left anterior descending and circumflex arteries. Marked ST segment elevation developed in leads I, aVL, and V3 to V6 concomitant with visible QT/T alternans in leads V4 and V5, and ventricular tachyarrhythmia was initiated. Brugada syndrome and vasospastic angina coexisted in this patient, and T wave alternans can be used as a predictor of ventricular tachyarrhythmias in such patients.     

Electrocardiographic detection of left ventricular hypertrophy using echocardiographic determination of left ventricular mass as the reference standard. Comparison of standard criteria, computer diagnosis and physician interpretation

Electrocardiographic findings of left ventricular hypertrophy were compared with echocardiographic left ventricular mass in 148 patients to assess performance of standard electrocardiographic criteria, the IBM Bonner program and physician interpretation. On echocardiography, 43% of the patients had left ventricular hypertrophy (left ventricular mass greater than 215 g). Sokolow-Lyon voltage-(S in V1 + R in V5 or V6) and Romhilt-Estes point score correlated modestly with left ventricular mass (r = 0.40, p less than 0.001 and r = 0.55, p less than 0.001, respectively). Sensitivity of Sokolow-Lyon voltage greater than 3.5 mV for left ventricular hypertrophy was only 22%, but specificity was 93%. Point score for probable left ventricular hypertrophy (greater than or equal to 4 points) had 48% sensitivity and 85% specificity, whereas definite hypertrophy (greater than or equal to 5 points) had 34% sensitivity and 98% specificity. Computer analysis resulted in 45% sensitivity and 83% specificity. Overall diagnostic accuracy of the IBM Bonner program (67%) was better than that of Sokolow-Lyon voltage (62%), but worse than the Romhilt-Estes point score (69% for greater than or equal to 4 points or 70% for greater than or equal to 5 points). Three cardiologists interpreted electrocardiograms independently and in a blinded fashion. Physician sensitivity was 56%, specificity 92% and accuracy 76%. Correlation with left ventricular hypertrophy was good (r = 0.70, p less than 0.001). It is concluded that: 1) computer diagnosis of left ventricular hypertrophy by the IBM Bonner program is no more accurate than diagnosis by Sokolow-Lyon or Romhilt-Estes criteria, and 2) physician recognition of left ventricular hypertrophy is more accurate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Determinants of mitral inflow velocity profiles in relation to left ventricular volume change: evaluations by pulsed Doppler echocardiography and left ventriculography]

We evaluated relationships between pulsed Doppler echocardiographic (PDE) parameters of flow velocity profiles across the mitral orifice and left ventriculographic (LVG) parameters of left ventricular volume changes. Subjects consisted of 19 patients with coronary artery disease and 12 patients with chest pain syndrome. Peak flow velocities at the rapid filling (E) and atrial contraction (A) were measured by PDE. Time constant of left ventricular relaxation (T), left ventricular minimum pressure (LVPmin), LV end-diastolic pressure (LVEDP) and pulmonary capillary wedge V wave pressure (PCW-V) were measured during cardiac catheterization. From the analysis of LVG, the rapid filling fraction (RFF), and the atrial filling fraction (AFF) were obtained. The left ventricular chamber stiffness (K) was identified by the analysis of the pressure-volume relationship of the left ventricle. We investigated the relationship between A/E and AFF/RFF by univariate linear regression analysis. We then performed stepwise multivariate linear regression analysis to predict E, A, A/E, RFF, AFF and AFF/RFF by the variables of left ventricular filling, i.e., T, LVPmin, LVEDP, PCW-V, K, heart rate (at the examination of PDE or LVG), mean arterial blood pressure (at PDE or LVG) and age. The A/E correlated significantly with AFF/RFF (r = 0.50, p < 0.01). The results of the multivariate linear regression analyses were as follows: [sequence: see text] The correlation of A/E and AFF/RFF were explained by some variables, except the variable T. The results of uni- and multivariate linear regression analyses showed that factors affecting the flow velocity profile across the mitral orifice did not account for the left ventricular volume changes. We also observed that, even in subjects with coronary heart disease, aging is a main factor that influences peak flow velocity at atrial contraction (A).     

A case of neurogenic myocardial stunning presenting transient left ventricular mid-portion ballooning simulating atypical takotsubo cardiomyopathy

A 57-year-old female patient, who was initially suspected to have subarachnoid hemorrhage, was admitted to our hospital. She experienced severe dyspnea and chest pain owing to pneumonia on the fourth admission day. Electrocardiography showed ST-segment elevation in leads V(2) through V(5), and echocardiography revealed hypokinetic left ventricular wall motion. No stenosis was found in the coronary arteries by urgent coronary angiography. However, left ventriculography revealed that the basal and apical areas were hyperkinetic and the mid portion was akinetic. After a month, left ventricular wall motion was improved and coronary artery spasm provocation tests were negative. Although the clinical course of this patient was similar to that of neurogenic myocardial stunning, the shape of her left ventricle was not typical.     

双心室起搏的临床疗效观察

目的　探讨缺血性或扩张型心肌病合并充血性心力衰竭行永久性双心室起搏治疗的临床效果。方法　对 1 0例缺血性或扩张型心肌病合并难治性心力衰竭和左束支阻滞患者 ,常规植入右心室起搏导线的同时植入冠状静脉窦电极导线于左室侧静脉、心大或心中静脉 ,行双心室同步起搏 (其中 2例为四腔起搏 )。通过临床观察、超声心动图测定及 6分钟平地行走评定对心功能的影响。结果　在充血性心力衰竭合并左束支阻滞患者植入冠状静脉窦电极导线行双心室起搏 ,产生较窄 QRS波 ,临床心功能从 ～ 级提高至 ～ 级 ( NYHA) ,同时使二尖瓣返流减少 ,射血分数提高 ,左室舒张末期内径缩小 ,6分钟平地行走距离比术前明显提高。结论　双心室起搏对难治性心力衰竭可能有辅助治疗作用。     

Cardiac physiology, biochemistry and morphology in response to excess growth hormone in the rat

The cardiac effects of excess growth hormone (GH) were studied in the intact adult rat and in tissues prepared from the rat. Female Wistar-Furth rats were inoculated with a clonal cell line of pituitary cells which secrete GH. Five weeks later, heart weight had increased 37% compared to control (P less than 0.01) due to concomitant increases in left and right ventricular weight. Hemodynamic measurements in the anesthetized rat showed that GH stimulated rats had a decrease in blood pressure and heart rate and a small increase of left ventricular end-diastolic pressure (P less than 0.05). Measurement of left ventricular contractility and relaxation, and response to beta-adrenergic stimulation were decreased in GH compared to control (P less than 0.05). Contractile protein biochemistry showed an 18% reduction in Ca2(+)-myosin ATPase activity of the left ventricle (P less than 0.05) and non-denaturing pyrophosphate gels of purified myosin demonstrated a significant shift of isoforms from the exclusive V1 pattern to both V1 and V3 isomyosins in both ventricles (P less than 0.05). In contrast to the physiological and protein biochemistry adaptations, left ventricular morphology by light microscopy and ultrastructure by electron microscopy were normal in the GH stimulated heart. There were no significant changes in myofibril fraction, in the myofibril to mitochondria ratio or in the capillary numerical density of the hypertrophied left ventricle (P = N.S.). This study demonstrates that under prolonged and extreme stimulation by GH, the heart undergoes considerable growth/hypertrophy. Although cardiac morphology remains normal during this growth, there are alterations of the isomyosins such that ATPase activity is diminished and ventricular function is decreased.