module 3 chapter 1a

32

Upload: deirdre-ramsey

Post on 30-Dec-2015

48 views

Category:

Documents


1 download

DESCRIPTION

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. - PowerPoint PPT Presentation

TRANSCRIPT

Page 1: Module 3 chapter 1a
Page 2: Module 3 chapter 1a

MODULE 3 CHAPTER 1AE-Hypertension Academy

Page 3: Module 3 chapter 1a

CARDIOVASCULAR CHANGES IN HYPERTENSION

Page 4: 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.

Page 5: Module 3 chapter 1a

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

Page 6: Module 3 chapter 1a

• 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

Page 7: Module 3 chapter 1a

• 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

Page 8: Module 3 chapter 1a

• Concentric left-ventricular hypertrophy, when a pressure load leads to growth in cardiomyocyte thickness

• Eccentric hypertrophy, when a volume load produces myocyte lengthening;

LVH

Page 9: Module 3 chapter 1a
Page 10: Module 3 chapter 1a

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

Page 11: Module 3 chapter 1a

Reactive increase in left ventricular mass in response to an increased workload

Lorell, Carabello. Circulation 2000;102:470–479Verdecchia 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 hypertrophyInduction of cellular proto- oncogenes

Increased ratio of wall thicknessto dimension

Cellular hypertrophyInduction of cellular proto- oncogenes

Increased ratio of wall thicknessto dimension

Left Ventricular Hypertrophy

Page 12: Module 3 chapter 1a

0

20

40

60

80

100

120

Stroke Heart failure Coronary disease

2-y

ea

r a

ge

-ad

jus

ted

in

cid

en

ce

(p

er

10

0 p

ati

en

ts)

Hypertension

Hypertension + LVH

LVH is an independent risk factor for stroke, heart failure

and Coronary Heart Disease

Page 13: Module 3 chapter 1a

• 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/m2 in men 95 gms/m2 in womenESC 2013

Page 14: Module 3 chapter 1a

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)

Page 15: Module 3 chapter 1a

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

Page 16: Module 3 chapter 1a

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

Page 17: Module 3 chapter 1a

ESC 2013

Page 18: Module 3 chapter 1a

• 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

Page 19: Module 3 chapter 1a

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

Page 20: Module 3 chapter 1a

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

Page 21: Module 3 chapter 1a

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

Page 22: Module 3 chapter 1a

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

Page 23: Module 3 chapter 1a

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

Page 24: Module 3 chapter 1a

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/1.73m2, 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 microalbuminuria be made on a spot urine sample

Page 25: Module 3 chapter 1a

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

Page 26: Module 3 chapter 1a

ESC 2013

Page 27: Module 3 chapter 1a

Investigations (ESC 2013)

Page 28: Module 3 chapter 1a

Investigations (ESC 2013)

Page 29: Module 3 chapter 1a

ESC 2013

Page 30: Module 3 chapter 1a

Summary

Page 31: Module 3 chapter 1a

Conclusion

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

Page 32: Module 3 chapter 1a

END OF MODULE 3 CHAPTER 1A