2. MODULE 3 CHAPTER 1A E-Hypertension Academy

3. CARDIOVASCULAR CHANGES IN HYPERTENSION

4. 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.

5. 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

6. 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 structural remodeling

7. 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 Hypertensive heart disease (HHD) The myocardial fibrosis

8. Concentric left-ventricular hypertrophy, when a pressure load leads to growth in cardiomyocyte thickness Eccentric hypertrophy, when a volume load produces myocyte lengthening; LVH

10. Picture from Atlas of the Heart Hurst JW et al eds. New York:Lippencot,1988. 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. LVH

11. Reactive increase in left ventricular mass in response to an increased workload Lorell, Carabello. Circulation 2000;102:470–479 Verdecchia et al. J Am Coll Cardiol 2001;38:1829–1835 Concentric Hypertrophy due to Persistent pressure overload Atherosclerosis Concentric Hypertrophy due to Persistent pressure overload Atherosclerosis Eccentric hypertrophy due to Na + and H2O retention Eccentric hypertrophy due to Na + and H2O retention Myocyte elongation Normal ratio of wall thickness to dimension Myocyte elongation Normal ratio of wall thickness to dimension Cellular hypertrophy Induction of cellular proto- oncogenes Increased ratio of wall thickness to dimension Cellular hypertrophy Induction of cellular proto- oncogenes Increased ratio of wall thickness to dimension Left Ventricular Hypertrophy

12. LVH is an independent risk factor for stroke, heart failure and Coronary Heart Disease

13. 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/m 2 in men 95 gms/m 2 in women ESC 2013

14. 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)

15. 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

16. 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/m 2

17. ESC 2013

18. Microvascular disease 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

19. 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

20. 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

21. 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

22. 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

23. 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

24. 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-Gault formula or, more recently, through the Chronic Kidney Disease EPIdemiology Collaboration (CKD-EPI) formula When eGFR is below 60 mL/min/1.73m 2, 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 microalbuminuria be made on a spot urine sample

25. 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

26. ESC 2013

27. Investigations (ESC 2013)

29. ESC 2013

30. Summary

31. Conclusion Detection of earliest cardiovascular changes in asymptomatic hypertensives and appropiriate management will prevent future CVD and kidney disease.

32. END OF MODULE 3 CHAPTER 1A