Prevent ion, Diagno s is , and
Trea tment of Hyp er t en s ive
Heart Disease
Vasiliki V. Georgiopoulou, MD,
Andreas P. Kalogeropoulos, MD, Paolo Raggi, MD,
Javed Butler, MD, MPH*
KEYWORDS

Hypertensive heart disease
Prevention
Treatment
Prolonged increase of blood pressure (BP) causes
a variety of changes in the myocardial structure,
coronary vasculature, and conduction system of
the heart, collectively known as hypertensive heart
disease (HHD). The resulting left ventricular
dysfunction, ischemia, and arrhythmias all
contribute to the high morbidity and mortality
burden, and health care cost related to HHD.
Controlling BP effectively reduces HHD complica-
tions, but BP control at the population levels has
largely been met with only modest success. More-
over, recent epidemiologic studies continue to
shift acceptable BP levels from what is usual in
the population to what is optimal for preventing
HHD-related complications.1,2
DEFINITION
Long-standing hypertension leads to complex
changes in cardiac chamber geometry and
myocardial composition, which in turn result in
the development of left ventricular hypertrophy
(LVH), ischemic heart disease, various conduction
abnormalities, and heart failure (HF) (with reduced
or preserved systolic function) (Box 1). These
changes are collectively referred to as HHD. In
the latest version of International Classification of
Diseases (ICD-10), hypertensive diseases have
been assigned multiple codes (I10eI15) to classify
the various forms of HHD including essential
hypertension, HHD with and without HF, combined
HHD and renal disease, and secondary hyperten-
sion.3 Pathophysiologically, HHD encompasses
Disclosures: None.
Division of Cardiology, Emory University, 1365 Clifton Road NE, Suite AT-430, Atlanta, GA 30322, USA
* Corresponding author.
E-mail address: javed.butler@emory.edu
Cardiol Clin 28 (2010) 675–691
doi:10.1016/j.ccl.2010.07.005
0733-8651/10/$ e see front matter Ó 2010 Elsevier Inc. All rights reserved.
both the direct and indirect effects of prolonged
uncontrolled hypertension; however, the term
HHD is clinically usually reserved for disease
states in which patients’ symptoms cannot be
attributed to an alternate cause. Thus, although
hypertension is clearly associated with coronary
disease, angina in the presence of obstructive
coronary stenosis may not be equated with HHD
because coronary disease can be attributable to
other simultaneous causes. However, angina
related to LVH and microvascular disease in
a patient with hypertension in the absence of
obstructive epicardial coronary stenosis can be re-
garded as HHD.
PATHOPHYSIOLOGY
The pathophysiology of HHD is a complex interplay
of hemodynamic, structural, cellular, neurohor-
monal, and molecular factors. Increased BP leads
to adverse changes in cardiac structure and func-
tion through increased afterload and neurohor-
monal and vascular changes. According to the
nature of the trigger stimulus, signal transduction
can occur in 2 directions. Cardiomyocytes either
undergo hypertrophy,4 an adaptive response in
an attempt to normalize systolic wall stress of the
ventricle, or apoptosis,5 a maladaptive process re-
sulting in dilatation and failure of the ventricle. Pres-
sure overload of the left ventricle (LV) and loss of
reciprocal regulation between profibrotic and anti-
cardiology.theclinics.com
fibrotic molecules is associated with increased