Left ventricular hypertrophy versus chronic kidney disease as predictors of cardiovascular events in hypertension: a Greek 6-year-follow-up study

Tsioufis, Costas; Vezali, Elena; Tsiachris, Dimitris; Dimitriadis, Kyriakos; Taxiarchou, E.; Chatzis, Dimitrios; Thomopoulos, Costas; Syrseloudis, Dimitris; Stefanadi, Elli; Mihas, Costas; Katsi, V.; Papademetriou, Vasilios; Stefanadis, Christodoulos

doi:10.1097/hjh.0b013e32832401ff

Cited by 57 publications

(42 citation statements)

References 46 publications

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“…Along these lines, we recently showed in hypertensives that the presence of both LVH and chronic kidney disease was associated with a 2.5-fold increase in coronary events, a 4-fold increase in stroke, whereas the presence of LVH alone was associated with a 2.5-fold higher risk for stroke [38]. …”

Section: Discussionmentioning

confidence: 99%

Parallel Deterioration of Albuminuria, Arterial Stiffness and Left Ventricular Mass in Essential Hypertension: Integrating Target Organ Damage

et al. 2011

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Background: Albuminuria, arterial stiffening and left ventricular hypertrophy (LVH) constitute target organ damage. We estimated whether increased urinary albumin excretion, assessed by albumin-to-creatine ratio (ACR), and carotid to femoral pulse wave velocity (c-f PWV) were accompanied by augmented left ventricular (LV) mass index (LVMI) in hypertension. Methods: In 428 non-diabetic untreated hypertensives (257 men, mean age = 52 years, office blood pressure (BP) = 146/93 mm Hg) the distributions of ACR and c-f PWV were split by the median (8 mg/g and 7.8 m/s, respectively). Results: Age, male sex, 24 h systolic BP, ACR and c-f PWV were the independent predictors of LVMI (R² = 0.478, p < 0.0001). Among patients with low ACR (n = 198), those with high c-f PWV (n = 84) compared to those with low c-f PWV (n = 114) were characterized by increased LVMI (by 8.9 g/m², p = 0.012) and prevalence of LVH (30 vs. 14%, p = 0.015). Similarly among patients with high ACR (n = 230), those with high c-f PWV (n = 123) compared to those with low c-f PWV (n = 107) exhibited heightened LVMI (by 13.6 g/m², p = 0.001). Conclusions: Increased ACR in conjunction with pronounced arterial stiffness is accompanied by augmented LV mass and higher LVH rates. Furthermore, the interrelationships between albuminuria, c-f PWV and LVMI suggest parallel target organ damage progression.

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Section: Discussionmentioning

confidence: 99%

Parallel Deterioration of Albuminuria, Arterial Stiffness and Left Ventricular Mass in Essential Hypertension: Integrating Target Organ Damage

et al. 2011

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“…[1][2][3][4][5] Among these manifestations of cardiac damage, particular attention has been devoted to LVH because this phenotype has been reported to be a powerful, independent predictor of cardiovascular (CV) events and all-cause mortality either in the general population or in hypertensive cohorts. 6,7 Although the pathogenesis of hypertensive LVH is not fully understood, a consistent body of evidence indicates that the severity of pressure overload, as better reflected by out-of-office than by in-office blood pressure (BP) levels, in combination with nonhemodynamic variables, including genetic, ethnic, and humoral factors, plays a pivotal role in its development. 8,9 Nonetheless, numerous reports have also shown that circadian variations in BP correlate to LVH independently of 24-hour ambulatory BP monitoring (ABPM) values.…”

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confidence: 99%

Nighttime Blood Pressure and New-Onset Left Ventricular Hypertrophy

et al. 2013

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Extensive echocardiographic investigations performed in the past 3 decades have shown that hypertensive heart disease includes a variety of anatomic and functional alterations, such as left ventricular hypertrophy (LVH), systolic/diastolic dysfunction, myocardial fibrosis, and left atrial and aortic dilatations. [1][2][3][4][5] Among these manifestations of cardiac damage, particular attention has been devoted to LVH because this phenotype has been reported to be a powerful, independent predictor of cardiovascular (CV) events and all-cause mortality either in the general population or in hypertensive cohorts. 6,7 Although the pathogenesis of hypertensive LVH is not fully understood, a consistent body of evidence indicates that the severity of pressure overload, as better reflected by out-of-office than by in-office blood pressure (BP) levels, in combination with nonhemodynamic variables, including genetic, ethnic, and humoral factors, plays a pivotal role in its development. 8,9 Nonetheless, numerous reports have also shown that circadian variations in BP correlate to LVH independently of 24-hour ambulatory BP monitoring (ABPM) values. Furthermore, earlier studies suggested that daytime BP, in particular BP values recorded during working hours, is more closely associated with LVH compared with nighttime BP. 10 More recently, however, numerous studies have shown that nighttime BP and nocturnal BP fall are stronger correlates of LVH than daytime or average 24-hour BP. 11,12Although a blunted decrease in nighttime BP (ie, nondipping status) has been associated with unhealthy conditions, including diabetes mellitus, metabolic syndrome, sleep apnea, cardiac or extracardiac organ damage, resistant hypertension, and an increased risk of CV morbidity and mortality, 13-15 this issue remains a source of debate. It is worthy of mention that a systematic review by Hansen et al 16 which included 25 856 hypertensive patients and 9641 individuals randomly recruited from the population revealed that nondipping status and increased night-to-day BP ratio were associated with higher all-cause mortality and CV events but added a marginal prognostic value over and beyond 24-hour BP.

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“…Left ventricular (LV) hypertrophy (LVH), either detected by electrocardiography or echocardiography, has been shown to be an independent predictor of nonfatal and fatal cardiovascular (CV) events as well as all-cause death in a variety of clinical settings including general population-based samples 1,2 and selected cohorts of hypertensive, [3][4][5] coronary artery disease, 6 chronic kidney disease, 7 and heart failure patients. 8 Thus, the accurate and cost-effective identification of LVH represents a clinical priority for stratifying individual CV risk.…”

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DoesQRSVoltage Correction by Body Mass Index Improve the Accuracy of Electrocardiography in Detecting Left Ventricular Hypertrophy and Predicting Cardiovascular Events in a General Population?

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Bombelli

et al. 2015

J of Clinical Hypertension

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The authors assessed the value of body mass index (BMI) correction of two electrocardiographic criteria in improving detection of left ventricular hypertrophy (LVH) and prediction of cardiovascular and all-cause mortality in the Italian study Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) population. At entry, 1549 patients underwent diagnostic tests, 24-hour ambulatory blood pressure (BP) monitoring, standard electrocardiography, and echocardiography. The BMI-corrected Cornell voltage and Sokolow-Lyon voltage criteria provided better results for detection of echocardiographic LVH as compared with unadjusted electrocardiographic parameters. Cornell voltage index, but not Sokolow-Lyon index, was associated with an increased risk of cardiovascular events (and allcause mortality). The adjusted risk of cardiovascular events related to one-standard deviation increment of BMI-corrected Cornell voltage was similar to that conferred by the uncorrected criterion in the total population, but outperformed in obese participants. These findings show that correction for BMI may improve the diagnostic accuracy of Cornell voltage index in detecting LVH and prediction of cardiovascular mortality in obese individuals.

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Left ventricular hypertrophy versus chronic kidney disease as predictors of cardiovascular events in hypertension: a Greek 6-year-follow-up study

Abstract: In hypertensive patients free of cardiovascular disease, CKD and LVH are both independent prognosticators of the composite end point of all-cause death and cardiovascular morbidity, whereas LVH but not CKD is a major predictor for stroke.

Cited by 57 publications

References 46 publications

Parallel Deterioration of Albuminuria, Arterial Stiffness and Left Ventricular Mass in Essential Hypertension: Integrating Target Organ Damage

Parallel Deterioration of Albuminuria, Arterial Stiffness and Left Ventricular Mass in Essential Hypertension: Integrating Target Organ Damage

Nighttime Blood Pressure and New-Onset Left Ventricular Hypertrophy

DoesQRSVoltage Correction by Body Mass Index Improve the Accuracy of Electrocardiography in Detecting Left Ventricular Hypertrophy and Predicting Cardiovascular Events in a General Population?

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