Bicuspid aortic valve with associated aortopathy, significant left ventricular hypertrophy or concomitant hypertrophic cardiomyopathy: A diagnostic and therapeutic challenge

Due to its prevalence of 0.5%to 2%in the general population,with a 75%predominance among men,bicuspid aortic valve is the most common congenital heart defect.It is frequently accompanied by other cardiac congenital anomalies,and clinical presentation can vary significantly,with stenosis being the most common manifestation,often resulting in mild to moderate concentric hypertrophy of the left ventricle.Echocardiography is the primary diagnostic modality utilized for establishing the diagnosis,and it is often the sole diagnostic tool relied upon by clinicians.However,due to the heterogeneous clinical presentation and possible associated anomalies(which are often overlooked in clinical practice),it is necessary to employ various diagnostic methods and persist in finding the accurate diagnosis if multiple inconsistencies exist.By employing this approach,we can effectively manage these patients and provide them with appropriate treatment.Through a clinical case from our practice,we provide an overview of the literature on bicuspid aortic valve with aortophaty and the possible association with hypertrophic cardiomyopathy,diagnostic methods,and treatment options.This review article highlights the critical significance of achieving an accurate diagnosis in patients with bicuspid aortic valve and significant left ventricular hypertrophy.It is crucial to exclude other possible causes of left ventricular outflow tract obstruction,such as sub-or supra-aortic obstructions,and hypertrophic cardiomyopathy.

Mitochondria and left ventricular hypertrophy

Introduction Left ventricular hypertrophy (LVH) is one of the vicious organ damages of essential hypertension.It contributes a lot to high mortality of essential hypertension due to sudden cardiac death,ventricular arrhythmia and heart failure.Many factors involve in the pathogenesis of hypertension-induced LVH including inherited variants as well as environmental factors.……

Anemia treatment and left ventricular hypertrophy in non-dialysis chronic kidney disease

To this day, the target hemoglobin level that minimizes cardiovascular risk in chronic kidney disease (CKD) patients remains unclear. When one examines the many randomized trials of epoetin therapy in aggregate, enhanced quality of life provides the most cogent argument for hemoglobin levels above 110 g/L. It remains unclear whether treatment of anemia improves longevity, or even a surrogate marker (such as left ventricular [LV] mass index), especially when applied at earlier phases of CKD.

DMP1 prevents osteocyte alterations,FGF23 elevation and left ventricular hypertrophy in mice with chronic kidney disease

During chronic kidney disease (CKD),alterations in bone and mineral metabolism include increased production of the hormone fibroblast growth factor 23 (FGF23) that may contribute to cardiovascular mortality.The osteocyte protein dentin matrix protein 1 (DMP1) reduces FGF23 and enhances bone mineralization,but its effects in CKD are unknown.We tested the hypothesis that DMP1 supplementation in CKD would improve bone health,prevent FGF23 elevations and minimize consequent adverse cardiovascular outcomes.We investigated DMP1 regulation and effects in wild-type (WT) mice and the Col4a3^-/- mouse model of CKD.Col4a3^-/- mice demonstrated impaired kidney function,reduced bone DMP1 expression,reduced bone mass,altered osteocyte morphology and connectivity,increased osteocyte apoptosis,increased serum FGF23,hyperphosphatemia,left ventricular hypertrophy (LVH),and reduced survival.Genetic or pharmacological supplementation of DMP1 in Col4a3^-/- mice prevented osteocyte apoptosis,preserved osteocyte networks,corrected bone mass,partially lowered FGF23 levels by attenuating NFAT-induced FGF23 transcription,and further increased serum phosphate.Despite impaired kidney function and worsened hyperphosphatemia,DMP1 prevented development of LVH and improved Col4a3^-/- survival.Our data suggest that CKD reduces DMP1 expression,whereas its restoration represents a potential therapeutic approach to lower FGF23 and improve bone and cardiac health in CKD.

Improved scoring system for the electrocardiographic diagnosis of left ventricular hypertrophy

BACKGROUND Left ventricular hypertrophy(LVH) is a common manifestation of cardiovascular disease and a risk factor for cardiovascular morbidity and mortality, but available methods for its electrocardiographic(ECG) diagnosis have limited accuracy.AIM To investigate findings associated with LVH on ECG and developed an improved system for the diagnosis of LVH.METHODS A cohort study comparing ECG data acquired within 30 days of transthoracic echocardiography(TTE) was performed. Multivariate regression analysis identified ECG findings associated with increased LV mass and mass index. A scoring system was derived and performance compared to established criteria for LVH.RESULTS Data from 5486 outpatients with TTEs and corresponding ECGs were included in the derivation cohort, 333(6.1%) of whom had LVH by TTE. In the primary regression analysis, findings associated with LVH were amplitudes of Q in V3, R in V6, S in V3, T in V6, P' in V1, P in V6, as well as R and T-axis discordance, R peak time in V6, QRS duration, weight, height, sex, and age. From this we derived a score consisting of 5 criteria, and validated it in an independent cohort of 910 patients. With a threshold of 1.5 points, sensitivity and specificity were67.9% and 81.4%, and 62.5% and 83.2% in the derivation and validation cohorts,respectively. With a threshold of 2 points, sensitivity and specificity were 42.3% and 93.0%, and 37.5% and 93.4% in these cohorts.CONCLUSIONS This score had superior sensitivity for detection of LVH by ECG while making a modest sacrifice in specificity compared to conventional criteria.

Effect of Salvia Miltiorrhiza Bge on Left Ventricular Hypertrophy and the Expression of Tumor Necrosis Factor-α in Spontaneously Hypertensive Rats

The effects of salvia miltiorrhiza Bge (SMB) on left ventricular hypertrophy (LVH) and the expression of tumor necrosis factor-α (TNF-α) in the left ventricle of spontaneously hypertensive rats and the action mechanism were investigated. Normal Wistar-kyoto (WKY) rats were used as negative control, and spontaneously hypertensive rats (SHR) were randomly assigned to receive pla- cebo or SMB. SMB (1 g/kg·d) was injected intraperitoneally for 12 weeks. Systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured. HE, VG and immunohistochemical staining combined with computed morphometry were employed to evaluate the cardiomyocyte size, diameter, the collagen volume fraction (CVF), perivascular circumferential area (PVCA), and tumor necrosis factor-α (TNF-α) expression in the left ventricular tissue. The results showed, as compared with WKY rats, the SBP, LVMI, cardiomyocyte size, diameter, CVF, PCVA, and TNF-α expression were increased markedly in the 20-week-old spontaneously hypertensive rats. SMB decreased LVMI (P<0.01), size of cardiomyocytes (P<0.01), collagen volume fraction (P<0.01), perivascular circum- ferential area (P<0.01), and TNF-α expression (P<0.01), but had no effect on SBP (P>0.05). It was suggested that chronic administration of SMB could inhibit and reverse the development of LVH in spontaneously hypertensive rats independent of BP. TNF-α may be involved in the reversal mecha- nism of LVH by SMB.

Effect of Xinjikang on left ventricular hypertrophy remodeling in hypertensive rats

Objective:To investigate the effects of Xinjikang on the left ventricular hypertrophy remodeling and myocardial activity in hypertension.Methods:Sixty Wistar rats were randomly divided into four groups.The pressure-loaded left ventricular hypertrophy model was established with abdominal aorta ligation method.Rats in A and B groups were intragastrically administered with physiological saline,while C and D groups were administered with Xinjikang and metoprolol,respectively.The changes in blood pressure.E/A ratio,myocardial pathological morphology,myocardial lipoperoxides and superoxide dismustase activity in four groups were observed and compared before and after treatment.Results:There were statistically significant differences in E/A ratio between C group after treatment and model group(P<0.05).while no difference was observed between A and D groups(P>0.05);after treatment the myocardial lipoperoxides and superoxide dismustase contents in C and D groups were improved significantly compared with model group(P<0.05).Conclusions:Xinjikang can improve myocardial injury,restore myocardial parenchyma and myocardial interstitial remodeling functions in hypertensive rats with the left ventricular hypertrophy.

Regional Heterogeneity in 3D Myocardial Shortening in Hypertensive Left Ventricular Hypertrophy: A Cardiovascular CMR Tagging Substudy to the Life Study

Background: Increased relative wall thickness in hypertensive left ventricular hypertrophy (LVH) has been shown by echocardiography to allow preserved shortening at the endocardium despite depressed LV midwall circumferential shortening (MWCS). Depressed MWCS is an adverse prognostic indicator, but whether this finding reflects reduced global or regional LV myocardial function, as assessed by three-dimensional (3D) myocardial strain, is unknown. Methods and Results: Cardiac Magnetic Resonance (CMR) tissue tagging permits direct evaluation of regional 3D intramyocardial strain, independent of LV geometry. We evaluated 21 hypertensive patients with electrocardiographic LVH in the LIFE study and 8 normal controls using 3D MR tagging and echocardiography. Patients had higher MR LV mass than normals (116 ± 40 versus 63 ± 6 g/m2, P = 0.002). Neither echocardiographic fractional shortening (32 ± 6 versus 33% ± 3%), LVEF (63% versus 64%) or mean end-systolic stress (175 ± 27 versus 146 ± 28 g/cm2) were significantly different, yet global MWCS was decreased by both echocardiography (13.4 ± 2.8 versus 18.2% ± 1.5%, P P P = 0.002) in LVH and greater in lateral and anterior regions versus septal and posterior regions ( P P P 0.60, P = 0.001 for both). Conclusions: In patients with hypertensive LVH, despite normal LV function via echocardiography or CMR, CMR intramyocardial tagging show depressed global MWCS while 3D MR strain revealed marked underlying regional heterogeneity of LV dysfunction.

Association Between Lipid Profiles and Left Ventricular Hypertrophy:New Evidence from a Retrospective Study

Objective To explore the association between lipid profiles and left ventricular hypertrophy in a Chinese general population.Methods We conducted a retrospective observational study to investigate the relationship between lipid markers[including triglycerides,total cholesterol,low-density lipoprotein cholesterol,high-density lipoprotein(HDL)cholesterol,non-HDL-cholesterol,apolipoprotein A-I,apolipoprotein B,lipoprotein[a],and composite lipid profiles]and left ventricular hypertrophy.A total of 309,400 participants of two populations(one from Beijing and another from nationwide)who underwent physical examinations at different health management centers between 2009 and 2018 in China were included in the cross-sectional study.7,475 participants who had multiple physical examinations and initially did not have left ventricular hypertrophy constituted a longitudinal cohort to analyze the association between lipid markers and the new-onset of left ventricular hypertrophy.Left ventricular hypertrophy was measured by echocardiography and defined as an end-diastolic thickness of the mterventricular septum or left ventricle posterior wall>11 mm.The Logistic regression model was used in the cross-sectional study.Cox model and Cox model with restricted cubic splines were used in the longitudinal cohort.Results In the cross-sectional study for participants in the highest tertile of each lipid marker compared to the respective lowest,triglycerides[odds ratio(OR):1.2S0,95%CI:1.060 to 1.474],HDL-cholesterol(OR:0.780,95%CI:0.662 to 0.918),and lipoprotein(a)(OR:1.311,95%C7:1.115 to 1.541)had an association with left ventricular hypertrophy.In the longitudinal cohort,for participants in the highest tertile of each lipid marker at the baseline compared to the respective lowest,triglycerides[hazard ratio(HR):3.277,95%C/:1.720 to 6.244],HDL-cholesterol(HR:0.516,95%C7:0.283 to 0.940),non-HDL-cholesterol(HR:2.309,95%C/:1.296 to 4.112),apolipoprotein B(HR:2.244,95%CI:1.251 to 4.032)showed an association with new-onset left ventricular hypertrophy.In the Cox model with forward stepwise selection,triglycerides were the only lipid markers entered into the final model.Conclusion Lipids levels,especially triglycerides,are associated with left ventricular hypertrophy.Controlling triglycerides level potentiate to be a strategy in harnessing cardiac remodeling but deserve to be furdier investigated.

Lifestyle Changes for Abdominal Obesity Prevention and Encouraging Fruit Consumption May Be Beneficial in Preventing Left Ventricular Hypertrophy in Sub-Saharan African and Maghreb

There is a growing body of evidence showing a close correlation between left ventricular mass with cardiovascular morbidity and overall mortality. Therefore, identifying the determinants of left ventricular hypertrophy can be of great importance for cardiovascular prevention, for prognosis and therapeutic intervention. Objective: To assess the prevalence and identify the independent determinants of echocardiographic left ventricular hypertrophy in The MA-Ghreb and Sub-Saharan Africa Left-Ventricul ArGEometry Study (MAG-SALVAGES) participants. Methods: The MAG-SALVAGES is a community based study in which 100 asymptomatic Black Sub-Saharan African (BSSA) and 189 white skin Maghreb within the age of 18 to 55 years underwent a resting echocardiography. Multivariate logistic regression analysis was utilized to identify the independent determinants of LVH left ventricular hypertrophy. Results: Men represented the majority of the enrolled participants: 173 (59.9%). Echocardiographic left ventricular hypertrophy was seen in 10 (3.5%) participants. Age ≥40 years, female gender, overall obesity, abdominal obesity, hypertension status and less fruit consumption were significantly associated with echocardiography left ventricular hypertrophy. After adjusting for confounding factors, age ≥40 years, female gender, abdominal obesity and less fruit consumption were independently and significantly associated with echocardiographic left ventricular hypertrophy, as illustrated in the following equation: Y = 0.36 + 0.162 age >40 years + 2.69 female gender + 2.52 abdominal obesity + 1.31 less fruit consumption. Conclusion: Lifestyle changes for the prevention of abdominal obesity and encouraging fruit consumption may be beneficial in preventing left ventricular hypertrophy.

Function of the CaMKII-ryanodine receptor signaling pathway in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia

BACKGROUND:Calcium calmodulin-dependent kinase II(CaMKII) can be more active in patients with left ventricular hypertrophy(LVH),which in turn causes phosphorylation of ryanodine receptors,resulting in inactivation and the instability of intracellular calcium homeostasis.The present study aimed to determine the effect of CaMKII-ryanodine receptor pathway signaling in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia.METHODS:Forty New Zealand rabbits were randomized into four groups(10 per group):sham group,LVH group,KN-93 group(LVH+KN-93),and ryanodine group(LVH+ryanodine).Rabbits in the LVH,KN-93,and ryanodine groups were used to establish a left ventricular hypertrophy model by the coarctation of the abdominal aorta,while those in the sham group did not undergo the coarctation.After eight weeks,action potentials(APs) were recorded simultaneously in the endocardium and epicardium,and a transmural electrocardiogram(ECG) was also recorded in the rabbit left ventricular wedge model.Drugs were administered to the animals in the KN-93 and ryanodine groups,and the frequency of triggered APs and ventricular tachycardia was recorded after the rabbits were given isoprenaline(1 μmol/L) and high-frequency stimulation.RESULTS:The frequency(animals/group) of triggered APs was 0/10 in the sham group,10/10 in the LVH group,4/10 in the KN-93 group,and 1/10 in the ryanodine group.The frequencies of ventricular tachycardia were 0/10,9/10,3/10,and 1/10,respectively.The frequencies of polymorphic ventricular tachycardia or ventricular fibrillation were 0/10,7/10,2/10,and 1/10,respectively.The frequencies of triggered ventricular arrhythmias in the KN-93 and ryanodine groups were much lower than those in the LVH group(P<0.05).CONCLUSIONS:KN-93 and ryanodine can effectively reduce the occurrence of triggered ventricular arrhythmia in rabbits with LVH.The CaMKII-ryanodine signaling pathway can be used as a new means of treating ventricular arrhythmia.

Combined superposition effect of hypertension and dyslipidemia on left ventricular hypertrophy

Background : Hypertension and dyslipidemia are considered reversible risk factors for cardiovascular disease. The purpose of this study was to explore the impact of traditional and nontraditional blood lipid profiles on the risk of left ventricular hypertrophy(LVH) and to explore the superposition effect of dyslipidemia combined with hypertension.Methods : Data on 9134 participants(53.5 ±10.3 years old) from the Northeast China Rural Cardiovascular Health Study(NCRCHS) were statistically analyzed. The blood lipid profile was measured by total cholesterol(TC), low-density lipoprotein cholesterol(LDL-C), high-density lipoprotein cholesterol(HDL-C), total glyceride(TG), and calculated nontraditional blood lipid indices including non-HDL-C, atherosclerosis index(AI), TC/HDL-C, and residual cholesterol(RC).Results : After the adjustment of age and gender, the odds ratios(ORs) of LVH in patients with hypertension, high LDL-C, high non-HDL-C, high AI, and high TC/HDL-C were 3.97(3.31– 4.76), 1.27(1.02– 1.59), 1.21(1.04– 1.39), 1.33(1.15– 1.53), and 1.42(1.22– 1.65), respectively. After full adjustment of potential confounding factors, high AI and TC/HDL-C were associated with LVH rather than traditional blood lipid indices.The combination of hypertension and nontraditional dyslipidemia(defined by high AI and TC/HDL-C) was associated with the highest risk of LVH, especially in participants under 45 years of age. The risk was more significant in men, 5.09-fold and 6.24-fold,respectively, compared with 3.66-fold and 4.01-fold in women.Conclusions : People with dyslipidemia defined by nontraditional blood lipid indices(high AI and high TC/HDL-C) and hypertension were more likely to develop LVH.

Plasma Norepinephrine and Hemorheology in Essential Hypertensive Patients with Different Patterns of Left Ventricular Hypertrophy

对80例不同类型高血压左室肥厚（LVH）患者的血浆去甲肾上腺素（NE）和血液流变学改变进行观察。结果显示，（1）向心性肥厚组（CH）高切变率下全血粘度（WBV230）显著升高；（2）不对称性室间隔肥厚组（ASH）血浆NE和收缩末期室壁应力（ESS）增高较明显；（3）多元回归分析显示，SBP，ESS和血浆NE是影响相对室壁厚度的重要因素。提示CH是一种对压力负荷过重而产生的代偿形式；ASH的形成除了负荷因素外血浆NE可能起更重要的作用。

Impact of 1,25-(OH)_2D_3 on Left Ventricular Hypertrophy in Type 2 Diabetic Rats

Objective To investigate the impact of 1, 25-(OH)2D3 on left ventricular hypertrophy(LVH) in type 2 diabetic rats. Methods Type 2 diabetic mellitus(DM) model rats were established by intraperitoneally injecting with 30 mg/kg streptozotocin. After 8 weeks, 19 male rats were identified as diabetic with left ventricular hypertrophy(LVH) by ultrasound examination, and randomly assigned into three groups: untreated(DM-LVH, n=7), treated with insulin(DM-LVH+INS, n=6), and treated with 1, 25-(OH)2D3(DM-LVH+VD, n=6). Healthy male rats were used as the controls group(n=6). The fasting blood glucose and the insulin level were determined weekly. The left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor level were determined by 4 weeks later. Results In the DM-LVH model group, the insulin level was significantly decreased compared with the non-diabetic control group(P<0.05), whereas the blood glucose, left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor expression were significantly increased(all P<0.05). In the DM-LVH+INS and DM-LVH+VD groups, the insulin levels were significantly increased compared with the DM-LVH model group(P<0.05), whereas the other parameters were significantly decreased(all P<0.05). Conclusion 1, 25-(OH)2D3 could reverse LVH in diabetic rats and that the mechanism may involve stimulating insulin secretion and reducing blood glucose via direct up-regulation of 1, 25-(OH)2D3-receptor expression.

ABNORMAL CORONARY FLOW RESERVE IN PATIENTSWITH LEFT VENTRICULAR HYPERTROPHY DUE TOHYPERTENSION

Obiective To measure coronary flow reserve (CFR) with angiography and computer-ass assisted technique in patients with left ventricular hypertrophy due to hypertension. Methods Coronary arterialdiameter, cross - sectional area and blood velocity of coronary flow in left anterior descending artery (LAD) andright coronary artery (RCA) were calculated with a computer in serial images of coronary angiography. Coronaryflow reserve was then measured in 22 patients with left ventricular hypertrophy due to hypertension (hypertropygroup) and 26 normal subjects (control group). Results Blood velocity and flow of both coronary arteries weresignificantly higher in hypertrophy group (LAD: n=22, RCA: n=14) than in control group (LAD: n=26, RCA:n=20) before intracoronary papaverine. However, blood velocity and flow of both coronary arteries were increasedsimilarly in both groups after intracoronary papaverine. Coronary flow reserve in hypertrophy group (LAD:CFR=2.2± 1.0, RCA： CFR= 2.9± 0.8) was significantly lower than in control group (LAD: CFR= 3.9± 2.1, RCA:CFR=5.5±2.0, all P<0.01). Conclusion The study indicates that coronary flow reserve is reduced in patientswith left ventricular hypertrophy due to hypertension which may be related to a higher coronary flow at restingstate.

The Effectand Mechanism of Forsinopril on Ventricular Hypertrophy of SHR and Left Ventricular Pressure overloading Rat

The effects and mechanism of long term angiotensin converting enzyme inhibitor (ACEI) Forsinopril on left ventricular hypertrophy of spontaneous hypertension rat (SHR) and left ventricular pressure overloading rat were studied. The left ventricular index (left ventricle weight/body weight) was used to evaluate left ventricular hypertrophy and the in situ hybridization to investigate the TGF β1 gene expression in left ventricle. The results showed that Forsinopril significantly decreased the left ventricular index of both SHR and left ventricle pressure overloading rat. Forsinopril reduced the integral photic density of TGF β1 gene statement from 2.836±0.314 to 1.91±0.217 ( P <0.01, n =8 ) of SHR rat and from 3.071±0.456 to 2.376±0.379 ( P <0.01, n =8) of left ventricular pressure overloading rat respectively. It was concluded that Forsinopril could prevent the occurrence of left ventricular hypertrophy and reduce the TGF-β1 gene expression in left ventricle of both SHR and left ventricular pressure overloading rat significantly.

Evaluation of the Patient with Incidental Left Ventricular Hypertrophy on Echocardiography

Left ventricular hypertrophy(LVH),or an increase in cardiac mass,usually refl ects pathologic adaptation to chronic pressure or volume loads.Physiologic adaptation in athletes as well as genetic,metabolic,and infi ltrative disorders may also result in increased cardiac mass.Given vast differences in prognosis and therapeutic options associated with different underlying conditions,the evaluation of patients with LVH necessitates a modern,comprehensive evaluation incorporating multimodality imaging.Herein we present a systematic approach to patients with incidental LVH.

Ultrasonic evaluation of the relationship between left ventricular hypertrophy or left ventricular geometry and endothelial function in patients with essential hypertension

Objective： To assess the relationship between left ventricular hypertrophy （LVH） or left ventricular geometry （LVG） and endothelial function in patients with essential hypertension （EH）. Methods： Seventy-six patients and 30 normal subjects were first examined by echocardiography. Brachial artery dilatation induced by reactive hyperemia （DIRH） or nitroglycerin （DING） was detected using high-resolution ultrasonography. Results： DIRH was lower in patients with hypertension than in the controls, and the decrease in DIRH was greater in the patients with LVH than that in patients without LVH （4.36±2.54% vs 8.56 ± 1.87 %; P 〈 0.0001）. There were no significant differences in age, serum concentrations of total cholesterol, triglycerides or sugar, blood pressure and the brachial artery dilatation induced by nitroglycerin between the two groups （P 〉 0.05）. While there was no significant difference in DIRH between the patients with normal left ventricular geometry or cardiac remodeling, the patients showing either eccentric or concentric left ventricular hypertrophy had lower DIRH than the patients with normal left ventricular geometry or cardiac remodeling. The DIRH was the lowest in patients with concentric hypertrophy. Although bivariate analysis showed that the left ventricular mass index （LVMI） correlated well with the brachial artery dilatation induced by reactive hyperemia, diastolic blood pressure and mean blood pressure （r=-0.61, P 〈 0.0001; r=0.27, P 〈 0.05; r=0.31, P 〈 0.05, respectively）, a multivariate stepwise regression demonstrated that LVMI correlated only with the brachial artery dilatation induced by reactive hyperemia. Conclusion： Left ventricular hypertrophy was related to endothelial dysfunction in essential hypertension. The endothelial dysfunction might be basic and important in the progression of left ventricular hypertrophy.

Refinement of total 12-lead QRS voltage criteria for diagnosing left ventricular hypertrophy

Objective: We sought to test the hypothesis that the total QRS voltage without either set of the limb leads (I, II, III) or (R, L, F) may be a better indicator of LVH as compared to the total QRS voltage. Background: The total 12 lead QRS voltage has been a validated electrocardiographic criterion for left ventricular hypertrophy (LVH), with an upper limit of175 mm. However, there is some redundancy in this measurement as the output of the limb leads is repeated because leads I, II, III, and R, L, F use the same three electrodes. Methods: 43 unselected, consecutive echocardiograms were examined for evidence of LVH by wall thickness. Electrocardiogram (ECG) of these patients within a week of the echocardiogram were then examined for the total 12 leads QRS voltage, minus I, II, III and total minus R, L, F voltages. ECG findings were then compared with corresponding echocardiographic dimensions. Results: A total QRS voltage of123 mmon ECG yielded a sensitivity of 73% and specificity of 67% for diagnosing LVH with 95% CI = 0.59 - 0.89, p = 0.007. Total minus (R, L and F) value of110 mmon ECG appears to give the best sensitivity (73%), specificity (72%), and accuracy (64% negative predictive value and 82% positive predictive value) for LVH. Conclusion: It appears that total QRS voltage minus either set of the limb leads, especially the total minus R, L and F is a better criterion, with110 mmbeing the best specific, sensitive and accurate index for diagnosing LVH.

Effect of Osteoprotegerin and XRCC3 Genes Polymorphisms with the Occurrence of Left Ventricular Hypertrophy in Hypertensive Patients

Background: High blood pressure is associated with adverse morphological and functional changes in the cardiovascular system, including left ventricular hypertrophy (LVH). Osteoprotegerin (OPG) is a member of the tumor necrosis factor receptor superfamily of cytokines. X-ray repair cross-complementing protein 3 (XRCC3) is involved in the repair pathway for double-strand breaks (DSBs). We assessed the association of osteoprotegerin and XRCC3 gene polymorphisms with the occurrence of left ventricular hypertrophy in hypertensive patients. Patients and methods: The study included 50 hypertensive patients: 25 with LVH (group A) and 25 without LVH (group B). All cases were subjected to complete history taking and clinical examination. ECG and echocardiography were done. LV mass was calculated to detect the presence or absence of LV hypertrophy. DNA was extracted from blood samples, and then, each DNA sample was amplified in PCRs, to detect osteoprotogrin and XRCC3 gene polymorphisms. Results: Mean age in the cases in group A is 63.12 years and in group B was 58.24 years with statistically significant difference between the two groups. The duration of the disease and SBP revealed statistically significant difference between the two groups. The LV mass index and E/A ratio revealed high statistically significant difference between the two groups. OPG sequence revealed no statistically significant difference between the two groups, but XRCC3 sequence revealed statistically significant difference. The age was a risk factor for LVH. Conclusion: Osteoprotogrin and XRCC3 genes polymorphism mutations may be associated with left ventricular hypertrophy in hypertensive patients.