Left Ventricular Responses to Acute Changes in Late Systolic Pressure Augmentation in Older Adults
Division of Cardiovascular Medicine, University of Wisconsin, Madison, Wisconsin American Journal of Hypertension
(Impact Factor: 2.85).
03/2013; 26(7). DOI: 10.1093/ajh/hpt043
Changes in the cardiovascular system with age may predispose older persons to development of heart failure with preserved ejection fraction. Vascular stiffening, aortic pressure augmentation, and ventricular-vascular coupling have been implicated. We explored the potential for acute reductions in late systolic pressure augmentation to impact left ventricular relaxation in older persons without heart failure.METHODS
Sixteen older persons free of known cardiovascular disease with the exception of hypertension had noninvasive tonometry and cardiac ultrasound to evaluate central augmentation index (AI) and diastolic function at baseline and after randomized, blinded administration of intravenous B-type natriuretic peptide (BNP) and hydralazine in a crossover design.RESULTSAI was significantly reduced after BNP (11.4±8.9 to -0.2±14.7%; P = 0.02) and nonsignificantly reduced after hydralazine (14.7±8.4% to 11.5±8.8%; P = 0.39). With decreased AI during BNP, a trend toward worsened myocardial relaxation by tissue Doppler imaging occurred (E' velocity pre- and post-BNP: 10.0±2.5 and 8.8±2.0cm/s, respectively; P = 0.06). There was a significant fall in stroke volume with BNP (68.5±18.3 to 60.9±18.1ml; P = 0.02), suggesting that changes in preload overwhelmed effects of afterload reduction on ventricular performance. With hydralazine, neither relaxation nor stroke volume changed.CONCLUSIONS
Acute changes in late systolic aortic pressure augmentation do not necessarily lead to improved systolic or diastolic function in older people. Preload may be a more important determinant of cardiac performance than afterload in older people with compensated ventricular function. The potential for changes in preload to impair rather than enhance left ventricular systolic and diastolic function in older people warrants further study.CLINICAL TRIALS REGISTRATIONThis study is registered at clinicaltrials.gov as NCT00204984.
Available from: Vasilios Gabriel Athyros
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ABSTRACT: Heart failure with preserved ejection fraction (HFpEF). Arterial hypertension (AH), arterial stiffness (AS), older age, and female gender are the main determinants of HFpEF, but several cardiac or extra-cardiac pathologies are also possible causes. The combined ventricular-vascular stiffening (abnormal left atrium-left ventricle coupling related to AS) is the main contributor of the increased prevalence of HFpEF in elderly persons, particularly elderly women, and in younger persons with AH. The hospitalization and mortality rates of HFpEF are similar to those of heart failure with reduced EF (HFrEF). However, although the prognosis of HFrEF has been substantially improved during the last 2 decades, the effective treatment of HFpEF remains an unmet need. Regimens effective in HFrEF have no substantial effect on HFpEF, because of different pathophysiologies of the 2 syndromes. Pipeline drugs seem promising, but it will take some years before they are commercially available. Aggressive treatment of noncardiac comorbidities seems to be the only option at hand. Treatment of anaemia, sleep disorders, chronic kidney disease (CKD), non-alcoholic fatty liver (NAFLD), atrial fibrillation, diabetes, and careful use of diuretics to reduce preload are effective to some degree. Statin treatment, despite the presence of dyslipidaemia, deserves special attention because it has been proven, mainly in small studies or post hoc analyses of trials, that it offers a substantial improvement in quality of life and a reduction in mortality rates. We need to urgently utilize these recourses to relieve a considerable part of the general population suffering from HFpEF, a deadly disease.
Current Vascular Pharmacology 11/2014; 12(999). DOI:10.2174/1570161112666141126150948 · 2.97 Impact Factor
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ABSTRACT: To examine the putative measures of arterial stiffness and the mechanisms of adverse effects of stiffness on blood pressure and target organ damage using data from comprehensive hemodynamic profiles obtained in the Framingham Heart Study and the Age, Gene/Environment Susceptibility-Reykjavik Study.
Once thought to be a consequence of longstanding hypertension, recent evidence suggests that aortic stiffness antedates and contributes to the pathogenesis of hypertension and target organ damage in the heart, brain, and kidneys. Carotid-femoral pulse-wave velocity (CFPWV) has emerged as the reference standard measure of aortic stiffness and a powerful predictor of cardiovascular disease risk. Augmentation index, a putative measure of arterial stiffness and wave reflection, has complex relations with stiffness and risk. Recent evidence suggests that wave reflection, which is a normal consequence of impedance mismatch between compliant aorta and stiff muscular arteries, is protective and limits the exposure of target organs to potentially harmful pulsatile energy. Aortic stiffening produces impedance matching that reduces wave reflection and exposes the microcirculation to excessive pulsatile stress, resulting in microvascular target organ damage and dysfunction.
CFPWV provides a powerful new tool for risk stratification and elucidation of the pathogenesis of target organ damage in hypertension.
Current Opinion in Nephrology and Hypertension 01/2015; 24(1):1-7. DOI:10.1097/MNH.0000000000000092 · 3.86 Impact Factor
Available from: Thais Coutinho
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ABSTRACT: Increased arterial stiffness leads to increased pulsatile load on the heart. We investigated associations of components of pulsatile load with a measure of left ventricular (LV) systolic function-global longitudinal strain (GLS), in a community-based cohort ascertained based on family history of hypertension.
Arterial tonometry and echocardiography with speckle tracking were performed in 520 adults with normal LV ejection fraction (EF) (age 67±9 years, 70% hypertensive) to quantify measures of pulsatile load (characteristic aortic impedance (Zc), total arterial compliance (TAC), and augmentation index (AI)) and GLS. The associations of log-Zc, log-TAC, and AI with GLS were assessed using sex-specific z-scores for each measure of arterial load.
In univariable analyses, higher Zc was associated with worse GLS (less negative) and higher TAC and AI were associated with better GLS (all P < 0.001). In a multivariable model including age, sex, heart rate (HR), LVEF, mean arterial load (systemic vascular resistance), and measures of pulsatile load, Zc remained associated with GLS (β = 0.28, P < 0.001), while the associations of TAC and AI were no longer significant (P > 0.5). Additional adjustment for cardiovascular risk factors and history of coronary heart disease and stroke did not attenuate the association of Zc with GLS; Zc, sex, HR, LVEF remained associated with GLS after stepwise elimination (all P < 0.001).
Greater proximal aortic stiffness, as manifested by a higher Zc, is independently associated with worse LV longitudinal function.
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American Journal of Hypertension 04/2015; 28(11). DOI:10.1093/ajh/hpv039 · 2.85 Impact Factor
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