Arterial hypertension is the commonest cause of cardiovascular death. It may lead to hypertensive heart disease (HHD) including heart failure (HF), ischemic heart disease (IHD) and left ventricular hypertrophy (LVH). There is no consensus among new HTN practice guidelines as to target treatment of blood pressure (BP) among various subpopulations of patients. However, most guidelines now target a BP < 150/90 for patients >80y, a BP < 140/90 for patients with diabetes or CVD and a BP < 130/80 if diabetes, albuminuria, or high stroke risk is present. In United States, 1 out of every 3 adults has high BP. About 69% of people with first heart attack, 77% with first stroke and 74% with HF have BP higher than 140/90 mmHg [
1].
Essential hypertension accounts for 90% of adult cases and secondary causes of hypertension for the remaining 10%. According to the Framingham Study, hypertension accounts for about 1/4 of HF cases, and the risk of HF is increased by 2-fold in men, and 3-fold in women, respectively. Finally, hypertension affects other target organs including kidneys, eyes and peripheral arteries [
2].
Left ventricular hypertrophy (LVH) is the response of myocytes to various stimuli leading to myocytes’ hypertrophy, which occurs as a compensatory response to increased afterload [
2]. It is defined as an increase in LV mass, assessed by postmortem measurements, electrocardiographic (ECG), echocardiographic and Cardiovascular Magnetic Resonance (CMR) criteria. Early echocardiographic studies defined LVH as an absolute LV mass (LVM) exceeding 250 g [
2]. Regression of LVH with antihypertensive treatment reduces the risk of stroke, myocardial infarction and all-cause mortality [
2]. There are two main patterns of LVH: a) concentric and b) eccentric LVH [
2]. Concentric LVH is considered, when LV mass increases by wall thickening in response to pressure overload, as often in middle aged and elderly patients, is associated with lower cardiac output and predicts poor prognosis. There is a pathway from hypertension to concentric LVH without focal scar [
3], hypertension to concentric LVH with focal scar [
4], concentric remodelling with myocardial infarction assessed by replacement fibrosis [
5], and concentric LVH with symptomatic vascular events and heart failure either with replacement scar [
6] or without [
7,
8]. Diastolic dysfunction and/or heart failure with preserved ejection fraction (HFpEF), due to remodelling of the extracellular matrix and increase in LV filling pressures, are common in concentric LVH [
9‐
14]. In eccentric LVH, there is an increase in LV mass without increased concentricity and is associated with higher cardiac output [
8] (Fig.
2). It has not been fully clarified why patients develop a specific LVH pattern, as a response to hypertension. Factors such as pressure, volume overload, ethnicity, gender, obesity and plasma renin levels, all seems to play a role [
2]; however, the clinical implications of various LVH patterns are still under evaluation. The aim of this review is to discuss the potential advantages and disadvantages of CMR over the currently used echocardiographic techniques and clarify its additive value in the evaluation of HHD.