scholarly journals The deletion polymorphism of the angiotensin I-converting enzyme gene is associated with target organ damage in essential hypertension.

1996 ◽  
Vol 7 (12) ◽  
pp. 2550-2558
Author(s):  
R Pontremoli ◽  
A Sofia ◽  
A Tirotta ◽  
M Ravera ◽  
C Nicolella ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Confidence Interval ◽  
Odds Ratio ◽  
Ventricular Hypertrophy ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Ace Gene

The activity of the renin-angiotensin-aldosterone system is thought to play a significant role in the development of target organ damage in essential hypertension. An insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene has recently been associated with increased risk for left ventricular hypertrophy and coronary heart disease in the general population. The D allele is associated with higher levels of circulating ACE and therefore may predispose to cardiovascular damage. The study presented here was performed to investigate the association between the ACE genotype, microalbuminuria, retinopathy, and left ventricular hypertrophy in 106 patients with essential hypertension. ACE gene polymorphism was determined by polymerase chain reaction technique. Microalbuminuria was evaluated as albumin-to-creatinine ratio (A/C) in three nonconsecutive first morning urine samples (negative urine culture) after a 4-wk washout period. Microalbuminuria was defined as A/C between 2.38 to 19 (men) and 2.96 to 20 (women). Hypertensive retinopathy was evaluated by direct funduscopic examination (keith-Wagener-Barker classification) and left ventricular hypertrophy by M-B mode echocardiography. The distribution of the DD, ID, and II genotypes was 27, 50, and 23%, respectively. The prevalence of microalbuminuria, retinopathy, and left ventricular hypertrophy was 19, 74, and 72% respectively. There were no differences among the three genotypes for age, known duration of disease, body mass index, blood pressure, serum glucose, uric acid, and lipid profile. DD and ID genotypes were significantly associated with the presence of microalbuminuria (odds ratio, 8.51; 95% confidence interval, 1.07 to 67.85; P = 0.019), retinopathy (odds ratio, 5.19; 95% confidence interval, 1.71 to 15.75; P = 0.005) and left ventricular hypertrophy (odds ratio, 5.22; 95% confidence interval, 1.52 to 17.94; P = 0.016). Furthermore, patients with DD and ID genotypes showed higher levels of A/C (3.6 +/- 0.9, DD; 2.6 +/- 0.7, ID; 0.9 +/- 0.2 mg/mmol, II; P = 0.0015 by analysis of variance) and increased left ventricular mass index (152 +/- 4.7, DD + ID versus 133 +/- 5.7 g/m2, II; P = 0.01) compared with II patients. The D allele was significantly more frequent in patients with microalbuminuria (odds ratio, 2.59; 95% confidence interval, 1.24 to 5.41; P = 0.013) and in those with retinopathy (odds ratio, 2.44; 95% confidence interval, 1.21 to 4.90; P = 0.015). Multiple regression analyses performed among the entire cohort of patients demonstrated that ACE genotype significantly and independently influences the presence of retinopathy, left ventricular hypertrophy, and microalbuminuria. In conclusion, the D allele of the ACE gene is associated with microalbuminuria as well as with retinopathy and left ventricular hypertrophy, and seems to be an independent risk factor for target organ damage in essential hypertension.

scholarly journals SERUM URIC ACID AND TARGET ORGAN DAMAGE IN ESSENTIAL HYPERTENSION AT MEDICINE DEPARTMENT OF GMC, BETTIAH, BIHAR

2020 ◽  
pp. 1-3
Author(s):  
Mahendra Kumar ◽  
Dharmendra Prasad ◽  
Parshuram Yugal ◽  
Debarshi Jana
Keyword(s):  
Uric Acid ◽  
Essential Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Serum Uric Acid ◽  
Ventricular Hypertrophy ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Hypertensive Patients

Background Hypertension is a major risk factor for cardiovascular mortality, as it acts through its effects on target organs, such as the heart and kidneys. Hyperuricemia increases cardiovascular risk in patients with hypertension. Objective To assess the relationship between serum uric acid and target organ damage (left ventricular hypertrophy and microalbuminuria) in untreated patients with essential hypertension. Patients and methods: A cross-sectional study was carried out in 130 (85 females, 45 males) newly diagnosed, untreated patients with essential hypertension. Sixty-five healthy age- and sex-matched non-hypertensive individuals served as controls for comparison. Left ventricular hypertrophy was evaluated by cardiac ultrasound scan, and microalbuminuria was assessed in an early morning midstream urine sample by immunoturbidimetry. Blood samples were collected for assessing uric acid levels. Results Mean serum uric acid was significantly higher among the patients with hypertension (379.7±109.2 μmol/L) than in the controls (296.9±89.8 μmol/L; P<0.001), and the prevalence of hyperuricemia was 46.9% among the hypertensive patients and 16.9% among the controls (P<0.001). Among the hypertensive patients, microalbuminuria was present in 54.1% of those with hyperuricemia and in 24.6% of those with normal uric acid levels (P=0.001). Similarly, left ventricular hypertrophy was more common in the hypertensive patients with hyperuricemia (70.5% versus 42.0%, respectively; P=0.001). There was a significant linear relationship between mean uric acid levels and the number of target organ damage (none versus one versus two: P=0.012). Conclusion These results indicate that serum uric acid is associated with target organ damage in patients with hypertension, even at the time of diagnosis; thus, it is a reliable marker of cardiovascular damage in our patient population.

scholarly journals ECHOCARDIOGRAPHIC LEFT VENTRICULAR HYPERTROPHY IN ISCHEMIC STROKE OR TIA: MORE THAN A SIMPLE TARGET ORGAN DAMAGE: PP.4.140

2010 ◽  
Vol 28 ◽  
pp. e90
Author(s):  
L Castilla Guerra ◽  
MC Fernandez Moreno ◽  
J Alvarez Suero ◽  
E Carmona Nimo ◽  
N Vargas ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ

scholarly journals Creatinine clearance and subclinical target organ damage in primary hypertension

1970 ◽  
Vol 32 (3) ◽  
pp. 30-33
Author(s):  
SK Das ◽  
SC Jha
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Creatinine Clearance ◽  
Ventricular Hypertrophy ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Primary Hypertension ◽  
Control Group ◽  
Hypertensive Patients

Introduction: Despite the widely recognized dangers of uncontrolled hypertension, the disease remains inadequately treated in the majority of patients. This may be, in large part, because of the asymptomatic nature of the disease for the first 15 to 20 years, even as it progressively damages the cardiovascular system. Therefore, assessment of hypertension related subclinical target-organ damage represents a key diagnostic procedure for the risk stratification of hypertensive patients. Methods: A prospective case control study of 40 cases (hypertensive patients with CCR<60) and 40 controls (hypertensive patients with CCR>60) was conducted in Tribhuvan University Teaching Hospital (TUTH). Renal function was estimated by the Cockcroft-Gault formula. Left ventricular hypertrophy was determined by echocardiography. Retinal vascular changes were evaluated by direct ophthalmoscopy. Microalbumin in urine was measured from spot morning sample. Results: The prevalence of Left ventricular hypertrophy (LVH), microalbuminuria and retinopathy in cases and control group was 55% VS 20% (P=.001), 50% VS 20% (P=.004) and 92.5% VS 52.5% (P=.001). Patients with microalbuminuria showed prevalence of LVH, CCR<60 and retinopathy as 78.57%, 71.43% and 100% respectively. There was high prevalence of grade I and grade II retinopathy in patients with low CCR Conclusions: Results show that a reduction in creatinine clearance and/or presence of microalbuminuria is a marker of subclinical organ damage in patients with primary hypertension and normal serum creatinine irrespective of BP load and other traditional risk factors. Keywords: Creatinine clearance; primary hypertension; subclinical; target organ damage. DOI: http://dx.doi.org/10.3126/joim.v32i3.4957 Journal of Institute of Medicine, December, 2010; 32:3 30-33

Abstract P402: Familial Clustering of Hypertensive Target Organ Damage in the Community

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Teemu J Niiranen ◽  
Honghuang Lin ◽  
Martin G Larson ◽  
Ramachandran S Vasan
Keyword(s):  
Risk Factors ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Hypertension Status ◽  
Heart Study ◽  
Familial Clustering

Prior studies suggest that hypertensive target organ damage (TOD) is a heritable trait. However, the risk that parental TOD confers on propensity for TOD in their offspring, and how hypertensive TOD clusters in the background of parental versus offspring hypertension status remain unclear. We studied 3238 Framingham Heart Study participants (mean age 39±8 years, 53% women) with available parental data on TOD. Parents and offspring underwent measurements for echocardiographic left ventricular hypertrophy, microalbuminuria, and conventional risk factors. Prevalence of any TOD (left ventricular hypertrophy or microalbuminuria) in participants with 0 and ≥1 parents with any TOD was 7% (131 of 1860) and 13% (173 of 1378), respectively ( P <0.001 for difference). As illustrated in the Figure , having ≥1 parent with TOD was associated with greater odds of TOD in offspring compared to individuals without parental TOD (multivariable-adjusted odds ratio [OR], 1.65; 95% confidence interval [CI], 1.27-2.14). Similarly, parental left ventricular hypertrophy was associated with offspring left ventricular hypertrophy (OR, 2.73; 95% CI 1.92-3.89) and parental albuminuria was related to offspring albuminuria (OR, 1.49; 95% CI 1.03-2.16). These associations remained robust upon additional adjustment for risk factors and in analyses of subgroups defined according to parental or offspring hypertension status ( Figure ). Overall our data suggest that familial clustering of TOD in the community is independent of blood pressure. Additional studies are warranted to confirm our observations.

Left Ventricular Hypertrophy Precedes Other Target-Organ Damage in Primary Aldosteronism

Hypertension ◽  
1997 ◽  
Vol 29 (3) ◽  
pp. 723-727 ◽  
Author(s):  
Yuji Shigematsu ◽  
Mareomi Hamada ◽  
Hideki Okayama ◽  
Yuji Hara ◽  
Yutaka Hayashi ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Primary Aldosteronism ◽  
Ventricular Hypertrophy ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ

scholarly journals Effects of irbesartan on phenotypic alterations in monocytes and the inflammatory status of hypertensive patients with left ventricular hypertrophy

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jingsi Zhang ◽  
Lina Yang ◽  
Yanchun Ding
Keyword(s):  
Ventricular Hypertrophy ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Hypertensive Patients ◽  
Inflammatory Status ◽  
Tnf Α

Abstract Background Circulating monocytes and tissue macrophages play complex roles in the pathogenesis of hypertension and the resulting target organ damage. In this study, we observed alterations in the monocyte phenotype and inflammatory state of hypertensive patients with left ventricular hypertrophy (LVH) and studied the effects of irbesartan in these patients. This study might reveal a novel mechanism by which irbesartan alleviates LVH, and it could provide new targets for the prevention and treatment of hypertensive target organ damage. Methods CD163 and CD206 expression on monocytes and IL-10 and TNF-α levels in the serum of hypertensive patients with or without LVH and of healthy volunteers were detected. Furthermore, we treated monocytes from the LVH group with different concentrations of irbesartan, and then, CD163, CD206, IL-10 and TNF-α expression was detected. Results We found, for the first time, that the expression of CD163, CD206 and IL-10 in the LVH group was lower than that in the non-LVH group and healthy control group, but the TNF-α level in the LVH group was significantly higher. Irbesartan upregulated the expression of CD163 and CD206 in hypertensive patients with LVH in a concentration-dependent manner. Irbesartan also increased the expression of IL-10 and inhibited the expression of TNF-α in monocyte culture supernatants in a concentration-dependent manner. Conclusions Our data suggest that inflammation was activated in hypertensive patients with LVH and that the monocyte phenotype was mainly proinflammatory. The expression of proinflammatory factors increased while the expression of anti-inflammatory factors decreased. Irbesartan could alter the monocyte phenotype and inflammatory status in hypertensive patients with LVH. This previously unknown mechanism may explain how irbesartan alleviates LVH. Trail registration The study protocols were approved by the Ethical Committee of the Second Affiliated Hospital of Dalian Medical University. Each patient signed the informed consent form.

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