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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.
• 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 6fold 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
Concentric Hypertrophy due to
Persistent pressure overload
Atherosclerosis
Eccentric hypertrophy due to
Na + and H2O retention
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
2-year age-adjusted incidence
(per 100 patients)
120
100
Hypertension
Hypertension + LVH
80
60
40
20
0
Stroke
Heart failure
Coronary 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/m2 in 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-toradius 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
ESC 2013
Hypertensive Heart Disease (HHD)
Vascular and other changes
• 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
• 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-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
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
ESC 2013
Investigations (ESC 2013)
Investigations (ESC 2013)
ESC 2013
Summary
Conclusion
• Detection of earliest cardiovascular changes in
asymptomatic hypertensives and appropiriate
management will prevent future CVD and
kidney disease.
END OF MODULE 3 CHAPTER 1A