Displaying publications 1 - 20 of 21 in total

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  1. Arcari L, Hinojar R, Engel J, Freiwald T, Platschek S, Zainal H, et al.
    Int J Cardiol, 2020 05 01;306:102-108.
    PMID: 32169347 DOI: 10.1016/j.ijcard.2020.03.002
    AIMS: Profound left ventricular (LV) hypertrophy with diastolic dysfunction and heart failure is the cardinal manifestation of heart remodelling in chronic kidney disease (CKD). Previous studies related increased T1 mapping values in CKD with diffuse fibrosis. Native T1 is a non-specific readout that may also relate to increased intramyocardial fluid. We examined concomitant T1 and T2 mapping signatures and undertook comparisons with other hypertrophic conditions.

    METHODS: In this prospective multicentre study, consecutive CKD patients (n = 154) undergoing routine clinical cardiac magnetic resonance (CMR) imaging were compared with patients with hypertensive (HTN, n = 163) and hypertrophic cardiomyopathy (HCM, n = 158), and normotensive controls (n = 133).

    RESULTS: Native T1 was significantly higher in all patient groups, whereas native T2 in CKD only (p 

    Matched MeSH terms: Hypertrophy, Left Ventricular/pathology
  2. Ahmad A, Sattar MA, Azam M, Khan SA, Bhatt O, Johns EJ
    PLoS One, 2018;13(2):e0189386.
    PMID: 29447158 DOI: 10.1371/journal.pone.0189386
    Left ventricular hypertrophy (LVH) is associated with decreased responsiveness of renal α1-adrenoreceptors subtypes to adrenergic agonists. Nitric oxide donors are known to have antihypertrophic effects however their impact on responsiveness of renal α1-adrenoreceptors subtypes is unknown. This study investigated the impact of nitric oxide (NO) and its potential interaction with the responsiveness of renal α1-adrenoreceptors subtypes to adrenergic stimulation in rats with left ventricular hypertrophy (LVH). This study also explored the impact of NO donor on CSE expression in normal and LVH kidney. LVH was induced using isoprenaline and caffeine in drinking water for 2 weeks while NO donor (L-arginine, 1.25g/Lin drinking water) was given for 5 weeks. Intrarenal noradrenaline, phenylephrine and methoxamine responses were determined in the absence and presence of selective α1-adrenoceptor antagonists, 5- methylurapidil (5-MeU), chloroethylclonidine (CeC) and BMY 7378. Renal cortical endothelial nitric oxide synthase mRNA was upregulated 7 fold while that of cystathione γ lyase was unaltered in the NO treated LVH rats (LVH-NO) group compared to LVH group. The responsiveness of renal α1A, α1B and α1D-adrenoceptors in the low dose and high dose phases of 5-MeU, CEC and BMY7378 to adrenergic agonists was increased along with cGMP in the kidney of LVH-NO group. These findings suggest that exogenous NO precursor up-regulated the renal eNOS/NO/cGMP pathway in LVH rats and resulted in augmented α1A, α1B and α1D adrenoreceptors responsiveness to the adrenergic agonists. There is a positive interaction between H2S and NO production in normal animals but this interaction appears absent in LVH animals.
    Matched MeSH terms: Hypertrophy, Left Ventricular/physiopathology*
  3. Fang F, Luo XX, Zhang Q, Azlan H, Razali O, Ma Z, et al.
    Europace, 2015 Oct;17 Suppl 2:ii47-53.
    PMID: 26842115 DOI: 10.1093/europace/euv130
    Biventricular (BiV) pacing was superior to right ventricular apical (RVA) pacing at extended follow-up in the Pacing to Avoid Cardiac Enlargement (PACE) trial. Early pacing-induced systolic dyssynchrony (DYS) might be related to mid-term result. However, it remains unknown whether early pacing-induced DYS can predict long-term reduction of left ventricular (LV) systolic function.
    Matched MeSH terms: Hypertrophy, Left Ventricular/diagnosis; Hypertrophy, Left Ventricular/etiology*; Hypertrophy, Left Ventricular/prevention & control*
  4. Sharma JN, Uma K, Yusof AP
    Int J Cardiol, 1998 Feb 28;63(3):229-35.
    PMID: 9578349 DOI: 10.1016/s0167-5273(97)00329-x
    We investigated the cardiac tissue kallikrein and kininogen levels, left ventricular wall thickness and mean arterial blood pressure of Wistar Kyoto and spontaneously hypertensive rats with and without streptozotocin-induced diabetes. The mean arterial blood pressure was highly elevated (P<0.001) in Wistar Kyoto diabetic and spontaneously hypertensive diabetic rats as compared with their respective controls. The cardiac tissue kallikrein and kininogen levels were reduced significantly (P<0.001) in diabetic Wistar Kyoto, spontaneously hypertensive and diabetic spontaneously hypertensive compared with Wistar Kyoto control rats. In addition, the left ventricular thickness was found to be increased (P<0.001) in diabetic Wistar Kyoto and spontaneously hypertensive rats in the presence and in the absence of diabetes. Our results indicate that reduced activity of the kinin-forming system may be responsible for inducing left ventricular hypertrophy in the presence of raised mean arterial blood pressure in diabetic and hypertensive rats. Thus, the kinin-forming components might have a protective role against the development of left ventricular hypertrophy. The possible significance of these findings is discussed.
    Matched MeSH terms: Hypertrophy, Left Ventricular/complications; Hypertrophy, Left Ventricular/physiopathology*
  5. Boon-Peng H, Mat Jusoh JA, Marshall CR, Majid F, Danuri N, Basir F, et al.
    PLoS One, 2016;11(3):e0148755.
    PMID: 26930585 DOI: 10.1371/journal.pone.0148755
    Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular morbidity and mortality, and a powerful predictor of adverse cardiovascular outcomes in the hypertensive patients. It has complex multifactorial and polygenic basis for its pathogenesis. We hypothesized that rare copy number variants (CNVs) contribute to the LVH pathogenesis in hypertensive patients. Copy number variants (CNV) were identified in 258 hypertensive patients, 95 of whom had LVH, after genotyping with a high resolution SNP array. Following stringent filtering criteria, we identified 208 rare, or private CNVs that were only present in our patients with hypertension related LVH. Preliminary findings from Gene Ontology and pathway analysis of this study confirmed the involvement of the genes known to be functionally involved in cardiac development and phenotypes, in line with previously reported transcriptomic studies. Network enrichment analyses suggested that the gene-set was, directly or indirectly, involved in the transcription factors regulating the "foetal cardiac gene programme" which triggered the hypertrophic cascade, confirming previous reports. These findings suggest that multiple, individually rare copy number variants altering genes may contribute to the pathogenesis of hypertension-related LVH. In summary, we have provided further supporting evidence that rare CNV could potentially impact this common and complex disease susceptibility with lower heritability.
    Matched MeSH terms: Hypertrophy, Left Ventricular/etiology; Hypertrophy, Left Ventricular/genetics*
  6. Sharma JN, Kesavarao U
    Pharmacology, 2002 Apr;64(4):196-200.
    PMID: 11893900 DOI: 10.1159/000056171
    We investigated the total urinary kallikrein levels, left-ventricular wall thickness and mean arterial blood pressure of nontreated and captopril-treated diabetic and nondiabetic spontaneously hypertensive rats. The mean arterial blood pressure was significantly elevated in diabetic spontaneously hypertensive rats as compared to nondiabetic spontaneously hypertensive rats. Captopril treatment caused a significant reduction in the arterial blood pressure of both nondiabetic and diabetic spontaneously hypertensive rats. The left-ventricular wall thickness was also significantly reduced in diabetic and nondiabetic spontaneously hypertensive treated with captopril as compared to nontreated diabetic and nondiabetic spontaneously hypertensive rats. The total urinary kallikrein levels were significantly raised in captopril-treated diabetic and nondiabetic spontaneously hypertensive rats against the values obtained from nontreated diabetic and nondiabetic spontaneously hypertensive rats. These results indicate that blood pressure reduction and left ventricular wall regression with captopril treatment might be due to enhanced renal kallikrein formation. The significance of these findings is discussed.
    Matched MeSH terms: Hypertrophy, Left Ventricular/pathology; Hypertrophy, Left Ventricular/physiopathology*; Hypertrophy, Left Ventricular/urine
  7. Masliza M, Daud SM, Khalid Y
    Ann Acad Med Singap, 2005 Dec;34(11):684-5.
    PMID: 16453041
    INTRODUCTION: The prevalence and severity of diastolic dysfunction (DD) among newly diagnosed hypertensives (NDHT) is not fully established. The aim of this study was to evaluate left ventricular diastolic function (LVDF) in patients with NDHT.

    MATERIALS AND METHODS: This study involved 396 subjects (198 NDHT, age and gender matched 198 normotensives; age, 30 to 50 years). Parameters of LVDF included Doppler-echocardiographic measurements of peak early (E) and late (A) diastolic velocities, E-wave deceleration time (DT) and isovolumetric relaxation time (IVRT). E/A ratio of <1 was taken as an indicative of DD.

    RESULTS: Patients with NDHT had reduced E/A ratio (1.27 +/- 0.41 vs 1.37 +/- 0.35, P <0.001) and shortened DT (180.0 +/- 40.0 ms vs 190.0 +/- 30.0 ms, P = 0.025). The peak A velocity and IVRT were increased in the NDHT group [(62.73 +/- 13.82 ms vs 58.26 +/- 12.40 ms, P = 0.002) and (90.0 +/- 20.0 ms vs 80.0 +/- 10.0 ms, P <0.001), respectively]. Peak E velocity was similar in both groups. The prevalence of DD was increased in the NDHT group, 18.6% (32) vs 3.4% (6), P <0.001. Of the 32 NDHT subjects who had DD, 84.4% (27) had no left ventricular hypertrophy (LVH) and 15.7% (5) had LVH. Diastolic function was negatively correlated with age, body mass index, systolic blood pressure, diastolic blood pressure and left ventricular mass index.

    CONCLUSION: Impairment in LVDF occurs in NDHT which may precede structural abnormalities. Hypertension, obesity, older age and LVH are associated with worsening of diastolic function.

    Matched MeSH terms: Hypertrophy, Left Ventricular/etiology
  8. Perak AM, Khan SS, Colangelo LA, Gidding SS, Armstrong AC, Lewis CE, et al.
    J Am Soc Echocardiogr, 2021 04;34(4):388-400.
    PMID: 33212181 DOI: 10.1016/j.echo.2020.11.002
    BACKGROUND: Little is known about the timing of preclinical heart failure (HF) development, particularly among blacks. The primary aims of this study were to delineate age-related left ventricular (LV) structure and function evolution in a biracial cohort and to test the hypothesis that young-adult LV parameters within normative ranges would be associated with incident stage B-defining LV abnormalities over 25 years, independent of cumulative risk factor burden.

    METHODS: Data from the Coronary Artery Risk Development in Young Adults study were analyzed. Participants (n = 2,833) had a mean baseline age of 30.1 years; 45% were black, and 56% were women. Generalized estimating equation logistic regression was used to estimate age-related probabilities of stage B LV abnormalities (remodeling, hypertrophy, or dysfunction) and logistic regression to examine risk factor-adjusted associations between baseline LV parameters and incident abnormalities. Cox regression was used to assess whether baseline LV parameters associated with incident stage B LV abnormalities were also associated with incident clinical (stage C/D) HF events over >25 years' follow-up.

    RESULTS: Probabilities of stage B LV abnormalities at ages 25 and 60 years were 10.5% (95% CI, 9.4%-11.8%) and 45.0% (95% CI, 42.0%-48.1%), with significant race-sex disparities (e.g., at age 60, black men 52.7% [95% CI, 44.9%-60.3%], black women 59.4% [95% CI, 53.6%-65.0%], white men 39.1% [95% CI, 33.4%-45.0%], and white women 39.1% [95% CI, 33.9%-44.6%]). Over 25 years, baseline LV end-systolic dimension indexed to height was associated with incident systolic dysfunction (adjusted odds ratio per 1 SD higher, 2.56; 95% CI, 1.87-3.52), eccentric hypertrophy (1.34; 95% CI, 1.02-1.75), concentric hypertrophy (0.69; 95% CI, 0.51-0.91), and concentric remodeling (0.68; 95% CI, 0.58-0.79); baseline LV mass indexed to height2.7 was associated with incident eccentric hypertrophy (1.70; 95% CI, 1.25-2.32]), concentric hypertrophy (1.63; 95% CI, 1.19-2.24), and diastolic dysfunction (1.24; 95% CI, 1.01-1.52). Among the entire cohort with baseline echocardiographic data available (n = 4,097; 72 HF events), LV end-systolic dimension indexed to height and LV mass indexed to height2.7 were significantly associated with incident clinical HF (adjusted hazard ratios per 1 SD higher, 1.56 [95% CI, 1.26-1.93] and 1.42 [95% CI, 1.14-1.75], respectively).

    CONCLUSIONS: Stage B LV abnormalities and related racial disparities were present in young adulthood, increased with age, and were associated with baseline variation in indexed LV end-systolic dimension and mass. Baseline indexed LV end-systolic dimension and mass were also associated with incident clinical HF. Efforts to prevent the LV abnormalities underlying clinical HF should start from a young age.

    Matched MeSH terms: Hypertrophy, Left Ventricular/epidemiology
  9. Amin OSM, Al-Bajalan SJ, Mubarak A
    Med Arch, 2017 Jun;71(3):193-197.
    PMID: 28974832 DOI: 10.5455/medarh.2017.71.193-197
    BACKGROUND: A variety of ECG changes occur as an aftermath of stroke. Prolongation of the QTc interval is a well-documented change. We analyzed QTc interval prolongation among patients with acute hemorrhagic strokes.

    METHODS: This observational study was conducted at the Emergency Department of Sulaymaniyah General Teaching Hospital and Shar Hospital from September 1st, 2014 to August 31st, 2015. Fifty patients who developed acute spontaneous hypertensive intracerebral hemorrhage (ICH) and 50 patients who developed acute non-traumatic subarachnoid hemorrhage (SAH) were included in the study. All patients underwent resting 12-lead ECG within half an hour of admission. The QTc interval was calculated and analyzed in those 100 patients.

    RESULTS: Females (62%) outnumbered males (38%) with a female to male ratio of 1.6:1. Forty percent of the patients were between 60-69 years of age. Hypertension was seen in 82% of patients while left ventricular hypertrophy was documented in 40% of patients. The QTc was prolonged in 38 patients (17 patients in the ICH group and 21 patients in the SAH group). In both groups, males demonstrated QTc prolongation more than females. However, there were no statistically significant gender difference between both groups and within the same group. There was a statistically significant association between SAH and QTc prolongation (p-value<0.001); the ICH group did not demonstrate any significant relationship with QTc prolongation.

    CONCLUSION: Prolongation in the QTc interval was "statistically" associated with acute SAH only. No gender difference was noted; whether this observation is clinically significant or not, it needs further analytic studies.

    Matched MeSH terms: Hypertrophy, Left Ventricular/complications
  10. Colangelo LA, Carroll AJ, Perak AM, Gidding SS, Lima JAC, Lloyd-Jones DM
    Psychosom Med, 2024 01 09;86(2):60-71.
    PMID: 38193784 DOI: 10.1097/PSY.0000000000001277
    OBJECTIVE: Depression is a risk factor for coronary heart disease and left ventricular hypertrophy (LVH) is a potent predictor of coronary heart disease events. Whether depression is associated with LVH has received limited investigation. This study assessed cross-sectional and 20-year longitudinal associations of depressive symptoms with LVH outcomes after accounting for important known confounders.

    METHODS: From 5115 participants enrolled in 1985-1986 in the Coronary Artery Risk Development in Young Adults Study, 2533 had serial measures of depressive symptoms and subsequent echocardiography to measure normal LV geometry, concentric remodeling, and LVH. The primary exposure variable was trajectories of the Center for Epidemiologic Studies Depression (CES-D) scale score from 1990-1991 to 2010-2011. Multivariable polytomous logistic regression was used to assess associations of trajectories with a composite LV geometry outcome created using echocardiogram data measured in 2010-2011 and 2015-2016. Sex-specific conflicting results led to exploratory models that examined potential importance of testosterone and sex hormone-binding globulin.

    RESULTS: Overall CES-D and Somatic subscale trajectories had significant associations with LVH for female participants only. Odds ratios for the subthreshold (mean CES-D ≈ 14) and stable (mean CES-D ≈ 19) groups were 1.49 (95% confidence interval = 1.05-2.13) and 1.88 (95% confidence interval = 1.16-3.04), respectively. For female participants, sex hormone-binding globulin was inversely associated with LVH, and for male participants, bioavailable testosterone was positively associated with concentric geometry.

    CONCLUSIONS: Findings from cross-sectional and longitudinal regression models for female participants, but not male ones, and particularly for Somatic subscale trajectories suggested a plausible link among depression, androgens, and LVH. The role of androgens to the depression-LVH relation requires additional investigation in future studies.

    Matched MeSH terms: Hypertrophy, Left Ventricular/epidemiology
  11. Cader RA, Ibrahim OA, Paul S, Gafor HA, Mohd R
    Int Urol Nephrol, 2014 Jun;46(6):1209-15.
    PMID: 24307428 DOI: 10.1007/s11255-013-0615-8
    PURPOSE: Cardiovascular disease is the leading cause of mortality in dialysis patients with left ventricular hypertrophy (LVH) being an important predictor of mortality. We wanted to determine the prevalence of LVH in peritoneal dialysis (PD) patients and factors contributing to it.

    METHODS: This is a cross-sectional study assessing LVH using echocardiogram in PD patients. Left ventricular mass index (LVMI) was calculated to determine LVH. Chronic fluid overload (overhydration) was assessed using the body composition monitor, and blood pressure (BP) was measured using 24-h ambulatory BP monitoring.

    RESULTS: Thirty-one patients (21 females:10 males, 48.97 ± 14.50 years and dialysis vintage 40.0 ± 28.9 months) were studied. More than two-thirds (77.4 %) were hypertensive, and a third (35.5 %) were diabetic. Baseline data included mean serum albumin (37.34 ± 4.43 g/l), weekly Kt/V (2.02 ± 0.23), residual renal function of 68 (0-880) ml and ultrafiltration of 1,606.9 ± 548.6 ml. Majority of patients (80.6 %) had LVH on echocardiogram with LVMI of 136.5 ± 37.8 g/m(2) and overhydration of 2.23 ± 1.77 l. Average systolic BP, diastolic BP and mean arterial pressure were 141.2 ± 23.3, 90.8 ± 19.7 and 107.6 ± 19.6 mmHg, respectively. Patients with LVH had a lower serum albumin (p = 0.003), were more overhydrated (p = 0.010) and were on higher number of anti-hypertensive agents (p ≤ 0.001). Predictors of LVMI were overhydration (p = 0.002), the presence of diabetes (p = 0.008) and the number of anti-hypertensive agents used (p = 0.026). However, overhydration (p = 0.007) was the main predictor of LVH on multivariate analysis.

    CONCLUSION: Overhydration is strongly associated with LVH in PD patients.

    Matched MeSH terms: Hypertrophy, Left Ventricular/etiology*; Hypertrophy, Left Ventricular/physiopathology
  12. Ahmad A, Sattar MA, Rathore HA, Abdulla MH, Khan SA, Abdullah NA, et al.
    Can J Physiol Pharmacol, 2014 Dec;92(12):1029-35.
    PMID: 25403946 DOI: 10.1139/cjpp-2014-0236
    This study investigated the role of α1D-adrenoceptor in the modulation of renal haemodynamics in rats with left ventricular hypertrophy (LVH). LVH was established in Wistar-Kyoto (WKY) rats with isoprenaline (5.0 mg · (kg body mass)(-1), by subcutaneous injection every 72 h) and caffeine (62 mg · L(-1) in drinking water, daily for 14 days). Renal vasoconstrictor responses were measured for noradrenaline (NA), phenylephrine (PE), and methoxamine (ME) before and immediately after low or high dose intrarenal infusions of BMY 7378, a selective α1D-adrenoceptor blocker. The rats with LVH had higher mean arterial blood pressure and circulating NA levels, but lower renal cortical blood perfusion compared with the control group (all P < 0.05). In the LVH group, the magnitude of the renal vasoconstrictor response to ME was blunted, but not the response to NA or PE (P < 0.05), compared with the control group (LVH vs. C, 38% vs. 50%). The magnitude of the drop in the vasoconstrictor responses to NA, PE, and ME in the presence of a higher dose of BMY 7378 was significantly greater in the LVH group compared with the control group (LVH vs. C, 45% vs. 25% for NA, 52% vs. 33% for PE, 66% vs. 53% for ME, all P < 0.05). These findings indicate an impaired renal vasoconstrictor response to adrenergic agonists during LVH. In addition, the α1D-adrenoceptor subtype plays a key role in the modulation of vascular responses in this diseased state.
    Matched MeSH terms: Hypertrophy, Left Ventricular/chemically induced; Hypertrophy, Left Ventricular/metabolism*; Hypertrophy, Left Ventricular/physiopathology
  13. Wan Muhaizan WM, Swaminathan M, Daud MS
    Malays J Pathol, 2004 Jun;26(1):59-63.
    PMID: 16196153
    Cardiac sarcoidosis is a disease of young adults. In most cases it presents with sudden death, arrhythmias, conduction disorders, heart failure or cardiomyopathy. The authors describe two cases of myocardial involvement by sarcoidosis that lead to death of the patients. Case one was a 26-year-old Indian man who was previously well and presented with sudden death. Autopsy showed nodules of sarcoid granuloma involving the heart, lungs and lymph nodes. Case two was a 47-year-old Indian lady who complained of reduced effort tolerance. Echocardiography showed that she had restrictive hypertrophic cardiomyopathy with heart failure. Seven months after initial presentation, she developed worsening of heart failure and died. Autopsy revealed involvement of the heart, lungs and liver by sarcoidosis.
    Matched MeSH terms: Hypertrophy, Left Ventricular/pathology
  14. Mohamed AL, Yusoff K, Muttalif AR, Khalid BAk
    Med J Malaysia, 1999 Sep;54(3):338-45.
    PMID: 11045060
    Sudden cardiac death is a known complication of acromegaly. Little is known of the exact mechanism leading to sudden cardiac death in these patients. Ventricular tachyarrhythmias may be an important cause. If this is so, clinical markers of ventricular tachyarrhythmias may be more common in this group of patients. The presence of these markers allow better risk stratification among acromegalic patients.
    Matched MeSH terms: Hypertrophy, Left Ventricular/ultrasonography
  15. Sharma JN, Kesavarao U, Yusof AP
    Immunopharmacology, 1999 Sep;43(2-3):129-32.
    PMID: 10596843 DOI: 10.1016/s0162-3109(99)00070-3
    The present investigation was aimed at evaluating the cardiac and total plasma kininogen levels, as well as LVWT in hypertensive and diabetic rats. STZ-induced diabetes produced a significant (P < 0.001) rise in mean arterial blood pressure (BP). The LVWT increased (P < 0.001) in SHR with and without diabetes) and diabetic WKYR. The cardiac tissue, as well as total plasma kininogen levels fell significantly (P < 0.001) in diabetic WKYR and SHR with and without diabetes compared to the control WKYR. These findings suggest that reduced kininogen levels may indicate a deficiency in kinin generation in the heart and in the peripheral circulation in diabetic and hypertensive rats. This effect may contribute to the development of LVH.
    Matched MeSH terms: Hypertrophy, Left Ventricular/etiology
  16. Ahmad A, Sattar MA, Azam M, Abdulla MH, Khan SA, Hashmi F, et al.
    PLoS One, 2016;11(5):e0154995.
    PMID: 27191852 DOI: 10.1371/journal.pone.0154995
    The purpose of the present study was to investigate the interaction between H2S and NO (nitric oxide) in the kidney and to evaluate its impact on the functional contribution of α1A and α1B-adrenoreceptors subtypes mediating the renal vasoconstriction in the kidney of rats with left ventricular hypertrophy (LVH). In rats the LVH induction was by isoprenaline administration and caffeine in the drinking water together with intraperitoneal administration of H2S. The responsiveness of α1A and α1B to exogenous noradrenaline, phenylephrine and methoxaminein the absence and presence of 5-methylurapidil (5-MeU) and chloroethylclonidine (CEC) was studied. Cystathione gamma lyase (CSE), cystathione β synthase (CBS), 3-mercaptopyruvate sulphar transferase (3-MST) and endothelial nitric oxide synthase (eNOS) were quantified. There was significant up regulation of CSE and eNOS in the LVH-H2S compared to the LVH group (P<0.05). Baseline renal cortical blood perfusion (RCBP) was increased (P<0.05) in the LVH-H2S compared to the LVH group. The responsiveness of α1A-adrenergic receptors to adrenergic agonists was increased (P<0.05) after administration of low dose 5-Methylurapidil in the LVH-H2S group while α1B-adrenergic receptors responsiveness to adrenergic agonists were increased (P<0.05) by both low and high dose chloroethylclonidine in the LVH-H2S group. Treatment of LVH with H2S resulted in up-regulation of CSE/H2S, CBS, and 3-MST and eNOS/NO/cGMP pathways in the kidney. These up regulation of CSE/H2S, CBS, and 3-MST and eNOS/NO/cGMP pathways enhanced the responsiveness of α1A and α1B-adrenoreceptors subtypes to adrenergic agonists in LVH-H2S. These findings indicate an important role for H2S in modulating deranged signalling in the renal vasculature resulting from LVH development.
    Matched MeSH terms: Hypertrophy, Left Ventricular/metabolism*
  17. Freestone B, Rajaratnam R, Hussain N, Lip GY
    Int J Cardiol, 2003 Oct;91(2-3):233-8.
    PMID: 14559136
    BACKGROUND: There are established differences in cardiovascular disease in different racial groups. Worldwide, the literature regarding the clinical epidemiology of atrial fibrillation in non-white populations is scarce.

    OBJECTIVES: To document the prevalence of atrial fibrillation (AF) in the multiracial population of Malaysia, and to describe the clinical features and management of these patients.

    SETTING: Busy city centre general hospital in Kuala Lumpur, Malaysia, over a 1-month period.

    SUBJECTS: One-thousand four hundred and thirty-five acute medical admissions, of whom 40 patients (2.8%) had AF.

    RESULTS: Of 1435 acute medical admissions to Kuala Lumpur General Hospital over the 4-week study period, 40 had AF (21 male, 19 female; mean age 65 years). Of these, 18 were Malay, 16 Chinese and six Indian. Nineteen patients had previously known AF (seven with paroxysmal AF) and 21 were newly diagnosed cases. The principal associated medical conditions were ischaemic heart disease (42.5%), hypertension (40%) and heart failure (40%). Dyspnoea was the commonest presentation, whilst stroke was the cause of presentation in only two patients. Investigations were under-utilised, with chest X-ray and echocardiography in only 62.5% of patients and thyroid function checked in 15%. Only 16% of those with previously diagnosed AF were on warfarin, with a further three on aspirin. Anticoagulant therapy was started in 13.5% of patients previously not on warfarin, and aspirin in 8%. Records of contraindications to warfarin were unreliable, being identified in only 25%. For those with known AF, 58% were on digoxin. For new onset AF, digoxin was again the most common rate-limiting treatment, initiated in 38%, whilst five patients with new onset AF were commenced on amiodarone. DC cardioversion was not used in any of the patients with new onset AF.

    CONCLUSION: Amongst acute medical admissions to a single centre in Malaysia the prevalence of AF was 2.8%. Consistent with previous similar surveys in mainly western (caucasian) populations, standard investigations in this Malaysian cohort were also inadequate and there was underuse of anticoagulation, medication for ventricular rate control and cardioversion to sinus rhythm.

    Matched MeSH terms: Hypertrophy, Left Ventricular/diagnosis; Hypertrophy, Left Ventricular/ethnology; Hypertrophy, Left Ventricular/therapy
  18. Sim Lam PPL, Reduan MFH, Jasni S, Shaari R, Shaharulnizim N, Nordin ML, et al.
    Comp Clin Path, 2020 Sep 28.
    PMID: 33013278 DOI: 10.1007/s00580-020-03170-4
    Feline polycystic kidney disease (PKD) is an inherited disorder caused by the mutation of PKD1 gene that eventually lead to the development of chronic kidney disease. The latter condition causes hypertension and eventually progress into congestive heart failure. Feline parvovirus (FPV) is a highly contagious and often fatal disease infecting cats and other members of Felidae. An 8-month-old female domestic shorthair cat was presented with complaint of wound dehiscence a day after ovarian hysterectomy procedure. The wound at the suture site appeared necrotic, purulent with foul smell. The cat was found to have diarrhoea during the fixation of suture breakdown and, later, was tested positive with parvovirus infection. Complete blood count revealed anaemia, neutrophilia, lymphopenia and thrombocytosis. Biochemistry profiles showed hypoproteinaemia and elevated of urea and creatinine. The cat was hospitalised, and symptomatic treatments were given. During hospitalisation, the cat showed symptoms of polydipsia and polyuria and found dead 2 days later. Post-mortem findings demonstrated the cat had oral ulceration, thoracic effusion, fibrinopleuropneumonia, pericardial effusion, left ventricular hypertrophy and right ventricular dilation, chronic passive liver congestion, mesenteric lymphadenomegaly, intestinal haemorrhage, adrenomegaly and polycystic kidney. Histopathological evaluation revealed fibrinous pleuropneumonia, pulmonary atelectasis, emphysema and oedema, hypertrophic cardiomyopathy, hepatic necrosis, splenic necrosis, intestinal necrosis, renal necrosis and renal polycystic. Staphylococcus aureus and Escherichia coli were isolated from bronchus swab and intestinal segment, respectively. Polymerase chain reaction (PCR) revealed parvovirus infection. The cat was definitely diagnosed with polycystic kidney disease concurrent with parvoviral and secondary bacterial infections.
    Matched MeSH terms: Hypertrophy, Left Ventricular
  19. Dharan SS, Kamaruddin NA
    J ASEAN Fed Endocr Soc, 2017;32(2):169-172.
    PMID: 33442102 DOI: 10.15605/jafes.032.02.12
    Acromegaly is a rare disease with an annual incidence of 3 to 4 cases in a million.1 Diagnosis is often delayed due to the slow progression of the disease. Persistent elevation of growth hormone (GH) in acromegaly causes a reduction in life expectancy by 10 years. Aside from multiple cardiovascular, respiratory and metabolic co-morbidities, it has also been proven to cause an increased incidence of cancer. The main treatment of acromegaly is surgical excision of the functioning pituitary adenoma. Multiple comorbidities, including obstructive sleep apnea (OSA), left ventricular hypertrophy (LVH) and soft tissue swelling, make surgery complicated, if not impossible. Medical therapy to reduce comorbidities may be indicated in certain situations. Somatostatin receptor ligands (SRL) are able to reduce, and possibly normalize, IGF-1 levels.2 Reduction of insulin-like growth factor-1 (IGF-1), the main mediator of GH, is able to resolve headache, sweating, fatigue and soft tissue swelling, and also reduce ventricular hypertrophy. This case report illustrates the successful use of the SRL octreotide LAR in treating acromegaly. It also confirms the observation from several case series that thyroid cancer is the most common malignancy in acromegaly.
    Matched MeSH terms: Hypertrophy, Left Ventricular
  20. Veeraveedu PT, Sanada S, Okuda K, Fu HY, Matsuzaki T, Araki R, et al.
    Biochem Pharmacol, 2017 Aug 15;138:73-80.
    PMID: 28450225 DOI: 10.1016/j.bcp.2017.04.022
    BACKGROUND AND PURPOSE: ST2 is one of the interleukin (IL)-1 receptor family members comprising of membrane-bound (ST2L) and soluble (sST2) isoforms. Clinical trials have revealed that serum sST2 levels predict outcome in patient with myocardial infarction or chronic heart failure (HF). Meanwhile, we and others have reported that ablation of ST2 caused exaggerated cardiac remodeling in both ischemic and non-ischemic HF. Here, we tested whether IL-33, the ligand for ST2, protects myocardium against HF induced by mechanical overload using ligand specific knockout (IL-33(-/-)) mice.

    METHODS AND RESULTS: Transverse aortic constriction (TAC)/sham surgery were carried out in both IL-33 and WT-littermates. Echocardiographic measurements were performed at frequent interval during the study period. Heart was harvested for RNA and histological measurements. Following mechanical overload by TAC, myocardial mRNA expressions of Th1 cytokines, such as TNF-α were enhanced in IL-33(-/-) mice than in WT mice. After 8-weeks, IL-33(-/-) mice exhibited exacerbated left ventricular hypertrophy, increased chamber dilation, reduced fractional shortening, aggravated fibrosis, inflammation, and impaired survival compared with WT littermates. Accordingly, myocardial mRNA expressions of hypertrophic (c-Myc/BNP) molecular markers were also significantly enhanced in IL-33(-/-) mice than those in WT mice.

    CONCLUSIONS: We report for the first time that ablation of IL-33 directly and significantly leads to exacerbate cardiac remodeling with impaired cardiac function and survival upon mechanical stress. These data highlight the cardioprotective role of IL-33/ST2 system in the stressed myocardium and reveal a potential therapeutic role for IL-33 in non-ischemic HF.

    Matched MeSH terms: Hypertrophy, Left Ventricular/physiopathology
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