Hypertensive heart disease

Last revised by Dr Joachim Feger on 11 Dec 2021

Hypertensive heart disease (HHD) refers to a condition covering morphological and physiological changes of the heart, the coronary arteries and the aorta.

Over 1.1 billion people worldwide, one-fourth of all men and one-fifth of all women suffer from hypertension and the condition is in control in less than 20% of the affected population. It is also the main risk factor and cause of hypertensive heart disease 1.

Conditions associated with hypertensive heart disease include the following 2:

Possible symptoms include dyspnea, angina, syncope, heart failure or even sudden cardiac death. However, in the initial stages, most patients will be asymptomatic 3.

Classical findings on examination include an abnormally sustained, enlarged or displaced apical impulse and an S4 gallop suggesting left ventricular hypertrophy 3.

Electrocardiogram (ECG) might detect atrial fibrillation and arrhythmias. Furthermore, it might show a prolonged terminal inverted P wave suggesting atrial enlargement or QRS voltage increases suggesting left ventricular hypertrophy 3.

If left untreated hypertensive heart disease can lead to the following potentially life-threatening conditions:

Hypertensive heart disease encompasses various structural and functional changes of the heart, in particular, the cardiac wall on a microscopic and macroscopic level including the development of myocardial fibrosis and cardiac chamber remodeling as ventricular hypertrophy, atrial enlargement as well as aortic root dilatation and alterations of the coronary circulation 2,3.

Usually one of the earlier adaptive changes of the heart in the response to increased peripheral vascular resistance and systemic hypertension is concentric left ventricular hypertrophy.  An increased wall tension stimulates sarcomere proliferation within the myocardium leading to cardiomyocyte hypertrophy and an increase of the wall thickness relative to the left ventricular chamber dimension according to Laplace’s equation 3. Concomitantly an increased deposition of fibrous tissue mainly fibrillar collagen occurs in the extracellular matrix of the heart causing increased stiffness of the myocardium or a decline in myocardial elasticity, thus diastolic dysfunction. A continuously ongoing collagen accumulation eventually leads to a decrease of effective myofibrillar density and failure in transmission of the contractile force of the myocardium and thus systolic dysfunction 2-4. At the point, when the myocardium is no longer capable to compensate for the increased afterload through hypertrophy the ventricle will dilate, at first focally as eccentric hypertrophy then globally and concomitantly ventricular function will decrease 3.

The main cause of hypertensive heart disease is elevated peripheral vascular resistance and arterial hypertension.

Classical imaging features of hypertensive heart disease include left ventricular hypertrophy and left atrial enlargement which can be visualized in echocardiography, cardiac CT and cardiac MRI.

Chest x-ray might show an enlargement of the cardiac silhouette or cardiothoracic ratio.

Echocardiography can provide a lot of information in respect to the heart including wall thickness, cardiac chamber dimensions, ejection fractionmass index as well as wall motion abnormalities.

In advanced examinations additional information include the following 4,5:

  • cardiac strain abnormalities
    • reduced longitudinal strain and circumferential strain
    • increased radial strain

Cardiac CT might be conducted to rule out any concomitant coronary artery disease.

In the setting of hypertensive heart disease it might show: 

  • a corkscrew appearance of the distal coronary segments
  • aortic root dilatation

Cardiac MRI can detect and aid in the characterization of left ventricular hypertrophy as well as provide information in respect to wall thickness, cardiac function including cardiac volumes and cardiac strain. Furthermore, it can detect focal or diffuse myocardial fibrosis and assess the expansion of the extracellular space as well as help rule out the important differential diagnosis utilizing cardiac tissue characterization 4,6-8:

  • cine SSFP
    • left ventricular hypertrophy
    • increased left ventricular mass
    • aortic root dilatation
  • MR tagging/MR feature tracking
    • cardiac strain abnormalities (reduced longitudinal and circumferential strain)
    • increased left ventricular torsion
  • perfusion imaging
    • diffuse thin circumferential perfusion defect indicating small vessel disease
  • T1 mapping
  • T2 mapping
    • normal unless concomitant inflammation is present
  • ECV
    • mild increases suggest fibrosis especially in the setting of concentric or eccentric hypertrophy

The radiological report should include a description of the following:

Adequate pharmacological antihypertensive therapy is the mainstay in the management leading to improved diastolic function and cardiovascular outcomes.

Angiotensin-converting enzyme (ACE) inhibitors, AT1 receptor antagonists and diuretics showed good results in the treatment with regression of left ventricular hypertrophy, myocardial fibrosis and an improvement in diastolic dysfunction 3,4,9,10. Concomitant ischemic heart disease, heart failure and atrial fibrillation or arrhythmias should be treated accordingly.

Another part of the management includes lifestyle modifications and the control of other cardiovascular risk factors.

Conditions that can mimic the presentation and/or the appearance of hypertensive heart disease:

Diagnosing diffuse myocardial fibrosis using T1 mapping and extracellular volume in the setting of hypertensive heart disease is anything but straightforward due to subtle elevations. In the absence of an accurately established local reference range, it is often difficult or even impossible to differentiate from normal individuals in the daily clinical environment.

However, in the context of other parameters, this can help in the diagnosis.

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