This study introduced the deep researches on the diagnosis of left ventricular hypertrophy by electrocardiogram (ECG) and cardiac ultrasound as well as treatment of the left ventricular hypertrophy due to hypertension including drug therapy and non drug therapy
Hypertrophy, Left Ventricular ; Cardiomegaly ; hypertension

An 18-year-old boy was admitted with chest discomfort, nausea, and dyspnea at rest. At the age of 3 years, he underwent muscle biopsy and dystrophin gene analysis owing to an enlarged calf muscle and elevated serum kinase level (6,378 U/L) without overt weakness; based on the results, Becker muscular dystrophy (BMD) was diagnosed. The dystrophin gene showed deletion of exons 45 to 49. He remained ambulant and could step upstairs without significant difficulties. A chest roentgenogram showed cardiomegaly (cardiothoracic ratio, 54%), and his electrocardiogram (ECG) showed abnormal ST-T wave, biatrial enlargement, and left ventricular hypertrophy. The 2-dimensional and M-mode ECGs showed a severely dilated left ventricular cavity with diffuse hypokinesis. The systolic indices were reduced, including fractional shortening (9%) and ejection fraction (19%). Despite receiving intensive medical treatment, he died from congestive heart failure 5 months after the initial cardiac symptoms. We report a case of BMD with early-onset dilated cardiomyopathy associated with deletion of exons 45 to 49. Early cardiomyopathy can occur in BMD patients with certain genotypes; therefore, careful follow-up is required even in patients with mild phenotypes of BMD.
Adolescent ; Biopsy ; Cardiomegaly ; Cardiomyopathies ; Cardiomyopathy, Dilated ; Dyspnea ; Dystrophin ; Electrocardiography ; Exons ; Genotype ; Heart Failure ; Humans ; Hypertrophy, Left Ventricular ; Muscles ; Muscular Dystrophy, Duchenne ; Nausea ; Phenotype ; Phosphotransferases ; Thorax

Dilated cardiomyopathy (DCMP) remains a life threatening disease in young patients and is often difficult to differentiate from myocarditis. Early recognition and treatment of DCMP are crucial for good prognoses in this patient population. The clinical course of patients with DCMP that result in cardiogenic shock varies according to the etiology as well as patient age. The volumetric expansion of the enlarged heart can compress adjacent structures causing a number of related symptoms, especially in infants with soft cartilaginous bronchi. Therapeutic strategies for treating these issues vary according to the type of complication encountered. We report a case of severe DCMP with sudden onset of massive cardiomegaly with heart failure complicated by bronchial obstruction in an infant.
Bronchi ; Bronchoconstriction ; Cardiomegaly* ; Cardiomyopathy, Dilated* ; Deoxycytidine Monophosphate ; Heart Failure ; Humans ; Infant* ; Myocarditis ; Prognosis ; Shock, Cardiogenic

Authors evaluated the electrocardiographic criteria of Minnesota Code (III-1, III-2) for the diagnosis of left and right ventricular hypertrophy in 93 cases of healthy peoples, 74 cases of left ventricular hypertrophy and 4 cases of right ventricular hypertrophy and following results were obtained. 1. By left ventricular hypertropy criteria (III-1), there were 5.4% of false positive and 14.9% of false negative cases. 2. By right ventricular hypertrophy criteria III-2), there were 24.7% of false positive and 20.0% of false negative cases. 3. Electrocardiographic diagnosis of ventricular hypertrophy by Minnesota Code (III-1, III-2) were more reliable criteria than many other criteria of ventricular hypertrophy.
Diagnosis* ; Electrocardiography ; Hypertrophy* ; Hypertrophy, Left Ventricular ; Hypertrophy, Right Ventricular ; Minnesota*

The present study was aimed to explore pathophysiological implications of nitric oxide in the development of left and right ventricular hypertrophy. To induce selective left and right ventricular hypertrophy, rats were made two-kidney, one clip (2K1C) hypertensive and treated with monocrotaline (MCT), respectively. Six weeks later, the hearts were taken and their ventricular tissue mRNA and protein expression of endothelial constitutive isoform of nitric oxide synthase (NOS) were determined by reverse transcription-polymerase chain reaction and Western blot analysis, respectively. In 2K1C hypertensive rats, the expression of NOS mRNA was increased in parallel with its proteins in the left ventricle, but not in the right ventricle. In MCT-treated rats, the expression of NOS mRNA and proteins were proportionally increased in the right ventricle, but not in the left ventricle. These results suggest that the expression of NOS is specifically increased in association with the ventricular hypertrophy, which may be a mechanism counteracting the hypertrophy.
Animals ; Blotting, Western ; Cardiomegaly ; Heart ; Heart Ventricles ; Hypertrophy ; Hypertrophy, Right Ventricular* ; Monocrotaline ; Nitric Oxide Synthase ; Nitric Oxide* ; Rats ; RNA, Messenger

BACKGROUND: In hypertrophic cardiomyopathy(HCM), which is known as genetic disease, severity and location of left ventricular hypertrophy(LVH) is variable. So we investigated additional modify role of angintensin-I converting enzyme(ACE) gene, which is known to be implicated in cardiac hypertrophy. ACE genotypes and degree of hypertrophy were determined in each subject. METHOD: 172 patients(37 HCM, 26 normotenisve LVH, 19 hypertenisve LVH, 79 normal control) were included in this study. Left ventricular mass index(LVMI) was calculated from electrocardiogram by Rautaharju equation, and LVH was defined as LVMI is above 131g/m2 in male or above 110g/m2 in female. In HCM group, extent of left ventricular hypertrophy was also assessed by Wigle's method. DNA was extracted from peripheral blood and ACE I/D polymorphism was confirmed by PCR method. RESULTS: Frequency of D/D genotype is significantly higher in normotensive LVH group(0.231) and in HCM group(0.243) than normal control group(0.076)(Fisher's exact test, p<0.05). There was no significant difference in genotype frequency between other groups. The mean LVMI(g/m2) and Wigle's LVH score was significantly higher in DD than II and ID(259.8+/-156.4g/m2 vs 176.6+/-56.2g/m2, p<0.05, t-test, 7.82+/-2.4 vs 5.35+/-1.9, p<0.05, Mann-Whitney test). LVMI and LVH score also exhibited increasing tendency toward II, ID DD genotypes. CONCLUSION: D allele of ACE gene contribute to the development of cardiac hypertrophy in HCM as well as normotensive LVH.
Alleles ; Cardiomegaly ; DNA ; Electrocardiography ; Female ; Genotype ; Humans ; Hypertrophy ; Hypertrophy, Left Ventricular ; Male ; Polymerase Chain Reaction

BACKGROUND: In hypertrophic cardiomyopathy(HCM), which is known as genetic disease, severity and location of left ventricular hypertrophy(LVH) is variable. So we investigated additional modify role of angintensin-I converting enzyme(ACE) gene, which is known to be implicated in cardiac hypertrophy. ACE genotypes and degree of hypertrophy were determined in each subject. METHOD: 172 patients(37 HCM, 26 normotenisve LVH, 19 hypertenisve LVH, 79 normal control) were included in this study. Left ventricular mass index(LVMI) was calculated from electrocardiogram by Rautaharju equation, and LVH was defined as LVMI is above 131g/m2 in male or above 110g/m2 in female. In HCM group, extent of left ventricular hypertrophy was also assessed by Wigle's method. DNA was extracted from peripheral blood and ACE I/D polymorphism was confirmed by PCR method. RESULTS: Frequency of D/D genotype is significantly higher in normotensive LVH group(0.231) and in HCM group(0.243) than normal control group(0.076)(Fisher's exact test, p<0.05). There was no significant difference in genotype frequency between other groups. The mean LVMI(g/m2) and Wigle's LVH score was significantly higher in DD than II and ID(259.8+/-156.4g/m2 vs 176.6+/-56.2g/m2, p<0.05, t-test, 7.82+/-2.4 vs 5.35+/-1.9, p<0.05, Mann-Whitney test). LVMI and LVH score also exhibited increasing tendency toward II, ID DD genotypes. CONCLUSION: D allele of ACE gene contribute to the development of cardiac hypertrophy in HCM as well as normotensive LVH.
Alleles ; Cardiomegaly ; DNA ; Electrocardiography ; Female ; Genotype ; Humans ; Hypertrophy ; Hypertrophy, Left Ventricular ; Male ; Polymerase Chain Reaction

BACKGROUND AND OBJECTIVES: Calcineurin-dependent transcriptional pathway has recently been implicated in cardiac hypertrophy. Whether calcineurin inhibition can prevent the development of pressure-overload left ventricular hypertrophy (LVH) is still controversial. To elucidate this issue, the effects of calcineurin inhibitors on the prevention of pressure-overload LVH were examined in mice. MATERIALS AND METHODS: Pressure overload was induced by transverse aortic contriction (TAC) in 57 ICR mice. Three different doses of CsA (TAC/CsA group, n=21) and FK506 (TAC/FK group, n=20) were administered subcutaneously from -2 to 14 days after surgery and 16 mice were treated with vehicle (TAC group). Another 60 mice were sham-operated and treated with CsA (CsA group, n=19), FK506 (FK group, n=18) or vehicle (Control group, n=23). RESULTS: Two weeks after TAC, the LV weight-to-body weight (LVW/BW) ratio was not significantly different among the Control, CsA and FK groups although it was greater in the TAC group (4.55+/-0.69 mg/g) than in the Control(2.78+/-0.70 mg/g) and other sham-operated groups (p<0.00005). Low-dose CsA (5 mg/kg/day) or FK506 (0.6 mg/kg/day) injection following TAC did not decrease the LVW/BW ratio. However, intermediate-dose and high-dose CsA (25 and 50 mg/kg/day) or FK506 (2 and 6 mg/kg/day) treatment prevented pressure-overload induced LVH and the degree of LVH inhibition was dose-dependent. Interstitial and/or perivascular fibrosis was remarkably decreased by the administration of intermediate and high doses of calcineurin inhibitors for 2 weeks following TAC. CONCLUSION: Taken together, calcineurin inhibitors, CsA and FK506, attenuated pressure-overload LVH response in a dose-dependent fashion. This data indicates that a calcineurin-dependent signaling pathway is crucial in the development of pressure-overload LVH.
Animals ; Calcineurin ; Cardiomegaly ; Cyclosporine ; Fibrosis ; Hypertrophy ; Hypertrophy, Left Ventricular* ; Mice ; Mice, Inbred ICR ; Myocardium ; Tacrolimus

An impaired smooth muscle cell (SMC) relaxation of coronary artery by alteration of K+ channels would be the most potential explanation for reduced coronary reserve in left ventricular hypertrophy (LVH), however, this possibility has not been investigated. We performed morphometrical analysis of the coronary artery under electron microscopy and measured Ca2+-activated K (KCa) currents and delayed rectifier K (Kdr) currents by whole-cell and inside-out patch-clamp technique in single coronary arterial SMCs from rabbits subjected to isoprenaline-induced cardiac hypertrophy. Coronary arterial SMCs underwent significant changes in ultrastructure. The unitary current amplitude and the open-state probability of KCa channel were significantly reduced in hypertrophy without open-time and closed-time kinetic. The concentration-response curve of KCa channel to Ca2+ is shifted to the right in hypertrophy. The reduction in the mean single channel current and increase in the open channel noise of KCa channel by TEA were more sensitive in hypertrophy. Kdr current density is significantly reduced in hypertrophy without activation and inactivation kinetics. The sensitivity of Kdr current on 4-AP is significantly increased in hypertrophy. This is the first study to report evidence for alterations of KCa channels and Kdr channels in coronary SMCs with LVH. The findings may provide some insight into mechanism of the reduced coronary reserve in LVH.
Cardiomegaly* ; Coronary Vessels* ; Hypertrophy ; Hypertrophy, Left Ventricular ; Kinetics ; Microscopy, Electron ; Myocytes, Smooth Muscle ; Noise ; Patch-Clamp Techniques ; Rabbits ; Relaxation ; Tea

To investigate the effects of leonurine(Leo) on abdominal aortic constriction(AAC)-induced cardiac hypertrophy in rats and its mechanism. A rat model of pressure overload-induced cardiac hypertrophy was established by AAC method. After 27-d intervention with high-dose(30 mg·kg~(-1)) and low-dose(15 mg·kg~(-1)) Leo or positive control drug losartan(5 mg·kg~(-1)), the cardiac function was evaluated by hemodynamic method, followed by the recording of left ventricular systolic pressure(LVSP), left ventricular end-diastolic pressure(LVESP), as well as the maximum rate of increase and decrease in left ventricular pressure(±dp/dt_(max)). The degree of left ventricular hypertrophy was assessed based on heart weight index(HWI) and left ventricular mass index(LVWI). Myocardial tissue changes and the myocardial cell diameter(MD) were measured after hematoxylin-eosin(HE) staining. The contents of angiotensin Ⅱ(AngⅡ) and angiotensin Ⅱ type 1 receptor(AT1 R) in myocardial tissue were detected by ELISA. The level of Ca~(2+) in myocardial tissue was determined by colorimetry. The protein expression levels of phospholipase C(PLC), inositol triphosphate(IP3), AngⅡ, and AT1 R were assayed by Western blot. Real-time quantitative PCR(qRT-PCR) was employed to determine the mRNA expression levels of β-myosin heavy chain(β-MHC), atrial natriuretic factor(ANF), AngⅡ, and AT1 R. Compared with the model group, Leo decreased the LVSP, LVEDP, HWI, LVWI and MD values, but increased ±dp/dt_(max) of the left ventricle. Meanwhile, it improved the pathological morphology of myocardial tissue, reduced cardiac hypertrophy, edema, and inflammatory cell infiltration, decreased the protein expression levels of PLC, IP3, AngⅡ, AT1 R, as well as the mRNA expression levels of β-MHC, ANF, AngⅡ, AT1 R, c-fos, and c-Myc in myocardial tissue. Leo inhibited AAC-induced cardiac hypertrophy possibly by influencing the RAS system.
Angiotensin II/metabolism* ; Animals ; Cardiomegaly/genetics* ; Gallic Acid/analogs & derivatives* ; Hypertrophy, Left Ventricular/pathology* ; Myocardium/pathology* ; Rats