Left Ventricular Diastolic Dysfunction Is Related to Oxidative Stress and Exercise Capacity in Hypertensive Patients with Preserved Systolic Function

Dekleva, Milica; Ćelić, Vera; Kostić, Nada; Penčić, Biljana; Ivanovic, Ana M.; Čaparević, Zorica

doi:10.1159/000095883

Cited by 20 publications

(28 citation statements)

References 42 publications

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“…Increased oxidative stress has been shown to contribute to impaired skeletal muscle vasodilation during exercise in healthy humans and animals without hypertension 15,16 . Studies in humans without heart failure have implicated the role of oxidative stress in endothelial dysfunction and exercise intolerance 17-19 , which was independent of blood pressure. Increased oxidative stress has also been implicated in the pathogenesis of insulin resistance and diabetes mellitus 20,21 .…”

Section: Discussionmentioning

confidence: 99%

Effects of Potassium Magnesium Citrate Supplementation on 24-Hour Ambulatory Blood Pressure and Oxidative Stress Marker in Prehypertensive and Hypertensive Subjects

Vongpatanasin

Peri-Okonny

Velasco

et al. 2016

The American Journal of Cardiology

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Diet rich in fruits, vegetables, and dairy products, known as the Dietary Approaches to Stop Hypertension (DASH) diet, is known to reduce BP in hypertensive patients. More recently, the DASH diet was shown to reduce oxidative stress in hypertensive and nonhypertensive humans. However, the main nutritional components responsible for these beneficial effects of the DASH diet remain unknown. Because the DASH diet is rich in potassium (K), magnesium (Mg), and alkali, we performed a randomized, double-blinded, placebo-controlled study to compare effects of KMg Citrate (KMgCit), K Chloride (KCl), and K Citrate (KCit) to allow dissociation of the three components of K, Mg, and Citrate on 24-hour ambulatory BP and urinary 8-isoprostane in hypertensive and prehypertensive subjects, using a randomized crossover design. We found that KCl supplementation for 4 weeks induced a significant reduction in nighttime SBP compared to placebo (116±12 vs. 121±15 mmHg, respectively, p < 0.01 vs. placebo) while KMgCit and KCit had no significant effect in the same subjects (118±11 and 119±13 mmHg respectively, p > 0.1 vs. placebo). In contrast, urinary 8-isoprostane was significantly reduced with KMgCit powder compared to placebo (13.5±5.7 vs. 21.1±10.5 ng/mgCr, respectively, p < 0.001) while KCl and KCit had no effect (21.4±9.1 and 18.3±8.4, respectively, p > 0.1 vs. placebo). In conclusion, our study demonstrated differential effects of KCl and KMgCit supplementation on BP and the oxidative stress marker in prehypertensive and hypertensive subjects. Clinical significance of the anti-oxidative effect of KMgCit remains to be determined in future studies.

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Section: Discussionmentioning

confidence: 99%

Effects of Potassium Magnesium Citrate Supplementation on 24-Hour Ambulatory Blood Pressure and Oxidative Stress Marker in Prehypertensive and Hypertensive Subjects

Vongpatanasin

Peri-Okonny

Velasco

et al. 2016

The American Journal of Cardiology

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“…However, the lack of correlation between changes in diastolic function with changes in HR and hemodynamic loading provides some evidence that there are alterations in intrinsic relaxation properties of the left ventricle. Evidence of some association between changes in FMD and indexes of diastolic function hint at a role for a shared mechanism, which could relate to oxidative stress (8,19,42), but this requires further investigation.…”

Section: Cardiac Changes In Response To Prolonged Intensive Exercisementioning

confidence: 99%

Changes in vascular and cardiac function after prolonged strenuous exercise in humans

Dawson

Whyte

Black

et al. 2008

Journal of Applied Physiology

112

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DJ. Changes in vascular and cardiac function after prolonged strenuous exercise in humans. J Appl Physiol 105: 1562-1568. First published August 21, 2008 doi:10.1152/japplphysiol.90837.2008.-Prolonged exercise has been shown to result in an acute depression in cardiac function. However, little is known about the effect of this type of exercise on vascular function. Therefore, the purpose of the present study was to investigate the impact of an acute bout of prolonged strenuous exercise on vascular and cardiac function and the appearance of biomarkers of cardiomyocyte damage in 15 male (32 Ϯ 10 yr) nonelite runners. The subjects were tested on two occasions, the day before and within an hour of finishing the London marathon (229 Ϯ 38 min). Function of the brachial and femoral arteries was determined using flow-mediated dilatation (FMD). Echocardiographic assessment of cardiac strain, strain rate, tissue velocities, and flow velocities during diastole and systole were also obtained. Venous blood samples were taken for later assessment of cardiac troponin I (cTnI), a biomarker of cardiomyocyte damage. Completion of the marathon resulted in a depression in femoral (P ϭ 0.04), but not brachial (P ϭ 0.96), artery FMD. There was no change, pre-vs. postmarathon, in vascular shear, indicating that the impaired femoral artery function was not related to hemodynamic changes. The ratio of peak early to atrial radial strain rate, a measure of left ventricular diastolic function, was reduced postmarathon (P ϭ 0.006). Postrace cTnI was elevated in 12 of 13 runners, with levels above the recognized clinical threshold for damage in 7 of these. In conclusion, when taken together, these data suggest a transient depression in cardiac and leg vascular function following prolonged intensive exercise. cardiovascular; exercise; marathon; ultrasound; troponins EPIDEMIOLOGICAL (7, 33) and experimental (18) evidence supports the public health message that exercise training and physical activity have substantial vascular and cardiac health benefits, with an ϳ30% reduction in cardiac risk (39). Despite this, it is clear that acute exercise transiently elevates the risk of cardiac events (37), or even sudden cardiac death (SCD) (40), in those at risk. The cardiovascular and physiological responses to prolonged exercise that are implicated in this transient period of increased cardiovascular risk are not well understood.Previously, we and others have demonstrated that marathon running results in a modest depression in cardiac function, primarily observed in indexes of left ventricular diastolic function (12,28,29). This is associated with the sporadic appearance of biomarkers of cardiomyocyte damage (10,12,26,28,29,34). However, the changes in cardiac function after prolonged strenuous exercise that occur in different planes of motion (radial, circumferential, and longitudinal) have not previously been studied.Vascular endothelial function reflects the health of the vessel wall. The dilator response to a 5-min ischemic period, termed flow-me...

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“…Patients with isolated diastolic dysfunction due to type 2 diabetes [55] and arterial hypertension [56] demonstrate maximal workloads that are 1.9 and 2.5 metabolic equivalents (METs), respectively, lower than matched controls without diastolic dysfunction. In another study, maximal workloads were more than 80 watts and maximal specific oxygen uptake 41% lower in patients with diastolic dysfunction than in normals [46] (Table 1).…”

Section: Diastolic Dysfunction and Exercise Capacitymentioning

confidence: 99%

Diastolic dysfunction in exercise and its role for exercise capacity

et al. 2008

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Diastolic dysfunction is frequent in elderly subjects and in patients with left ventricular hypertrophy, vascular disease and diabetes mellitus. Patients with diastolic dysfunction demonstrate a reduced exercise capacity and might suffer from congestive heart failure (CHF). Presence of symptoms of CHF in the setting of a normal systolic function is referred to as heart failure with normal ejection fraction (HFNEF) or, if evidence of an impaired diastolic function is observed, as diastolic heart failure (DHF). Reduced exercise capacity in diastolic dysfunction results from a number of pathophysiological alterations such as slowed myocardial relaxation, reduced myocardial distensibility, elevated filling pressures, and reduced ventricular suction forces. These alterations limit the increase of ventricular diastolic filling and cardiac output during exercise and lead to pulmonary congestion. In healthy subjects, exercise training can enhance diastolic function and exercise capacity and prevent deterioration of diastolic function in the course of aging. In patients with diastolic dysfunction, exercise capacity can be enhanced by exercise training and pharmacological treatment, whereas improvement of diastolic function can only be observed in few patients.

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Left Ventricular Diastolic Dysfunction Is Related to Oxidative Stress and Exercise Capacity in Hypertensive Patients with Preserved Systolic Function

Cited by 20 publications

References 42 publications

Effects of Potassium Magnesium Citrate Supplementation on 24-Hour Ambulatory Blood Pressure and Oxidative Stress Marker in Prehypertensive and Hypertensive Subjects

Effects of Potassium Magnesium Citrate Supplementation on 24-Hour Ambulatory Blood Pressure and Oxidative Stress Marker in Prehypertensive and Hypertensive Subjects

Changes in vascular and cardiac function after prolonged strenuous exercise in humans

Diastolic dysfunction in exercise and its role for exercise capacity

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