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E-Hypertension Academy. Module 3 chapter 1a. Cardiovascular changes in Hypertension. Introduction. Clinical squeal of hypertension include heart failure, arrhythmias, and ischemic events, especially myocardial infarction and stroke.
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E-Hypertension Academy Module 3 chapter 1a
Introduction • Clinical squeal of hypertension include heart failure, arrhythmias, and ischemic events, especially myocardial infarction and stroke. • Recognizing the hypertensive heart has diagnostic as well as prognostic implications.
Hypertensive heart disease (HHD) The Sequel • Heart failure: reduced EF as well as Preserved EF • The link between HHD and atrial fibrillation, whose likelihood increases by 40% to 50% in the presence of hypertension • Ventricular arrhythmias occur more frequently in hypertensive patients , with QT dispersion increasing directly with left ventricular (LV) mass • Increased susceptibility to ischemic heart disease rounds out the cardiovascular squeal of HHD, with a 6-fold higher risk of myocardial infarction in hypertensive patients than in normotensive individuals
Hypertensive heart disease (HHD) The structural remodeling • Cardiomyocyte hypertrophy is but one of many structural alterations in HHD • Fibroblasts undergo hyperplasia and conversion to myofibroblasts, along with hypertrophy of vascular smooth muscle cells. • Noncellular elements central to myocardial remodeling in HHD include expansion of interstitial and perivascular collagen that make up the extracellular matrix. • Changes in intramyocardial capillary density and arteriolar thickening compound ischemia in the hearts of patients with hypertension
Hypertensive heart disease (HHD) The myocardial fibrosis • A common end point of many cellular and non cellular pathologic processes in HHD is myocardial fibrosis. • Fibrosis quantification in endomyocardial samples obtained via transjugular biopsy showed significantly greater collagen volume fraction in patients with hypertension than in normotensive controls
LVH • Concentric left-ventricular hypertrophy, when a pressure load leads to growth in cardiomyocyte thickness • Eccentric hypertrophy, when a volume load produces myocyte lengthening;
LVH • Left ventricular hypertrophy (LVH) is a condition wherein the cardiac muscle responds to increased resistance in the circulation by becoming enlarged • Fibers of the hypertrophied heart muscle become thickened and shortened, and consequently less able to relax. The outcome of this process is a heart that is less able to meet the output demands of normal circulation. Picture from Atlas of the Heart Hurst JW et al eds. New York:Lippencot,1988.
Left Ventricular Hypertrophy Reactive increase in left ventricular mass in response to an increased workload Eccentric hypertrophy due to Na + and H2O retention Concentric Hypertrophy due to Persistent pressure overload Atherosclerosis Cellular hypertrophy Induction of cellular proto- oncogenes Increased ratio of wall thickness to dimension Myocyte elongation Normal ratio of wall thickness to dimension Lorell, Carabello. Circulation 2000;102:470–479 Verdecchia et al. J Am Coll Cardiol 2001;38:1829–1835
LVH is an independent risk factor for stroke, heart failure and Coronary Heart Disease
Echocardiography can be used to estimate both Left ventricular mass and volume Since the two-dimensional images contain cross-sectional data, volume may be estimated from the short and long axes in systole or diastole LV MASS INDEX : 115gms/m2in men 95 gms/m2 in women ESC 2013
LVH – Measurement by Echo • Calculation of LV Mass (LVM) is currently performed according to the American Society of Echocardiography formula • Relative wall thickness (RWT) or the wall-to-radius ratio (2 x posterior wall thickness/end diastolic diameter) categorizes geometry (concentric or eccentric)
Three types of LVH • Concentric : RWT and LVM increased • Eccentric: RWT normal LVM increased • Concentric remodeling: RWT increased LVM normal • Concentric LVH is the strongest predictor of increased risk
Left Atrium • As witness to chronically elevated LV filling pressures, left atrial enlargement is a reliable marker of diastolic dysfunction in the absence of mitral valve disease • The correlation between left atrial volume and brain natriuretic peptide levels further underscores its role as sentinel in heart failure with preserved ejection fraction • LA volumes not only predict future HF especially HFPEF but also atrial fibrillation • Normal LA volume index is less than 22ml/m2
Hypertensive Heart Disease (HHD) Vascular and other changes • Microvasculardisease and endothelial dysfunction are apparent in hypertensive heart disease • Progressive impairment of flow-mediated vasodilation happens as LV mass increased, consistent with the previously described ultra structural remodeling of myocardial micro vessels • This explains increased frequency of hypertension in patients with chest pain, angiographically normal coronary arteries, and subendocardial ischemia on perfusion imaging
Hypertensive heart disease (HHD) Vascular and other changes • At the macrovascular level, increased arterial stiffness often seen in long-standing hypertension accelerates aortic pulse wave velocity . • This, in turn, results in earlier return of the wave reflected at the iliac bifurcation in systole, increasing LV afterload and central pulse pressure. • The concomitant fall in central diastolic blood pressure decreases coronary perfusion, further contributing to myocardial ischemia
Pulse Wave Velocity • Carotid-femoral PWV is the ‘gold standard’ for measuring aortic stiffness . • Although the relationship between aortic stiffness and events is continuous, a threshold of >10 m/s has been suggested as a conservative estimate of significant alterations of aortic function in middle-aged hypertensive patients
Ankle-Brachial Index (ABI) • Ankle-brachial index (ABI) can be measured either with automated devices, or with a continuous-wave Doppler • Unit and a BP Sphygmomanometer. • A low ABI (i.e. <0.9 signals PAD and, in general, advanced atherosclerosis, has predictive value for CV events , and was associated with approximately twice the 10-year CV mortality and major coronary event rate, compared with the overall rate in each Framingham category
Carotid Arteries • Ultrasound examination of the carotid arteries with measurement of intima media thickness (IMT) and/or the presence of plaques has been shown to predict the occurrence of both stroke and myocardial infarction independently of traditional CV risk factors • Carotid IMT >0.9mm has been taken as a conservative estimate of existing abnormalities
Fundoscopy • Grade III (retinal haemorrhages, microaneurysms, hard exudates, cotton wool spots) and grade IV retinopathy (grade III signs and papilloedema and/or macular oedema) are indicative of severe hypertensive retinopathy, with a high predictive value for mortality
Kidney • The diagnosis of hypertension-induced renal damage is based on the finding of a reduced renal function and/or the detection of elevated urinary excretion of albumin • Once detected, CKD is classified according to eGFR, calculated by the abbreviated ‘modification of diet in renal disease’ (MDRD) formula [208], the Cockcroft-Gaultformula or, more recently, through the Chronic Kidney Disease EPIdemiology Collaboration (CKD-EPI) formula • When eGFR is below 60 mL/min/1.73m2, it predicts not only future kidney disease but also future CVD • Therefore it is recommended, in all hypertensive patients, that eGFR be estimated and that a test for microalbuminuriabe made on a spot urine sample
Brain • Hypertension, beyond its well known effect on the occurrence of clinical stroke, is also associated with the risk of asymptomatic brain damage noticed on cerebral MRI, in particular in elderly individuals • White matter hyperintensities and silent infarcts are associated with an increased risk of stroke, cognitive decline and dementia • In hypertensive patients without overt CVD, MRI showed that silent cerebrovascular lesions are even more prevalent (44%) than cardiac (21%) and renal (26%) subclinical damage and do frequently occur in the absence of other signs of organ damage
Conclusion • Detection of earliest cardiovascular changes in asymptomatic hypertensives and appropiriate management will prevent future CVD and kidney disease.
