Cardiac Complications

Arterial hypertension is one of the main risk factors for cardiovascular diseases, as it imposes a chronic hemodynamic overload on the heart. The increase in blood pressure forces the left ventricle to work against elevated peripheral resistance, leading to structural and functional adaptations that can eventually progress to heart failure.

Left ventricular hypertrophy represents the initial compensatory response to increased afterload. The rise in blood pressure forces the myocardium to generate a greater contractile force to maintain an adequate cardiac output. This results in a progressive thickening of the ventricular walls, which can ultimately lead to ventricular dysfunction.

Stages of Left Ventricular Hypertrophy

Initial stage: concentric hypertrophy → The left ventricle develops uniform wall thickening to counteract increased vascular resistance. At this stage, the ventricular cavity volume remains nearly normal, but the rigidity of the walls reduces diastolic filling.
Advanced stage: eccentric hypertrophy → If hemodynamic stress persists, a progressive dilation of the ventricular cavity occurs to compensate for the reduced filling volume. This phase marks the transition to a pathological condition, with diastolic dysfunction and a tendency toward heart failure.
Terminal stage: diastolic and systolic dysfunction → The dilated ventricle becomes less efficient, the myocardium undergoes fibrosis, and ejection fraction progressively declines, leading to overt heart failure.

Electrocardiography (ECG) may reveal signs of left ventricular hypertrophy, such as increased QRS complex voltage and left-axis deviation. However, the gold standard for diagnosis remains echocardiography, which allows the measurement of myocardial thickness. Interventricular septal thickness greater than 10 mm is considered pathological, although it must be interpreted according to the patient's body size.

Left ventricular hypertrophy not only compromises ventricular function but also increases left atrial pressure. Over time, this leads to left atrial dilation, resulting in electrical remodeling and a higher predisposition to supraventricular arrhythmias, particularly atrial fibrillation (AF).
AF in hypertensive patients is a significant thromboembolic risk factor, increasing the likelihood of ischemic events, including stroke.

Myocardial hypertrophy associated with arterial hypertension leads to increased oxygen consumption and reduced coronary reserve. This, combined with the vascular alterations typical of hypertension, such as coronary atherosclerosis and endothelial dysfunction, exposes the patient to a higher risk of ischemic heart disease, which may manifest as:

Angina pectoris: due to reduced coronary perfusion in response to exertion.
Myocardial infarction: resulting from the rupture of an atherosclerotic plaque and the formation of coronary thrombi.
Chronic ischemic heart disease: characterized by a progressive reduction in myocardial function due to prolonged ischemia.

If left untreated, arterial hypertension can progress to heart failure, following two main pathophysiological trajectories:

Heart failure with preserved ejection fraction (HFpEF): the left ventricle is hypertrophic and stiff, with reduced filling capacity and increased left atrial pressure. It manifests with exertional dyspnea and pulmonary congestion.
Heart failure with reduced ejection fraction (HFrEF): the myocardium progressively weakens, reducing its contractile ability and leading to a decreased ejection fraction, with a high risk of overt heart failure.

Conclusion

Arterial hypertension is a primary risk factor for cardiovascular diseases, requiring constant monitoring and timely treatment to prevent the progression of cardiac damage. Management includes blood pressure control with antihypertensive medications, reducing myocardial overload, and preventing ischemic and arrhythmic complications.

References

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Gerdts E, et al. Left ventricular hypertrophy in hypertension: mechanisms, clinical implications, and treatment. J Hum Hypertens. 2024;38(5):399-408.
Bruno RM, et al. Arterial stiffness and hypertensive heart disease: a bidirectional pathophysiological interplay. Hypertension. 2023;81(2):857-868.
Regitz-Zagrosek V, et al. Gender differences in hypertensive heart disease. Curr Hypertens Rep. 2023;25(3):215-223.
Rossi GP, et al. Secondary hypertension and hypertensive heart disease: diagnostic and therapeutic challenges. J Hypertens. 2024;42(7):1234-1245.