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, over time, may evolve into heart failure.
Left ventricular hypertrophy represents the initial compensatory response to increased afterload. The rise in arterial pressure requires the myocardium to generate greater contractile force to ensure adequate cardiac output. This leads to progressive thickening of the ventricular walls, which can ultimately result in ventricular dysfunction.
Stages of Left Ventricular Hypertrophy
Early stage: concentric hypertrophy → The left ventricle develops uniform wall thickening to face increased vascular resistance. In this stage, the ventricular cavity volume remains nearly normal, but wall stiffness reduces diastolic filling.
Advanced stage: eccentric hypertrophy → If hemodynamic stress persists, there is progressive dilation of the ventricular cavity to compensate for reduced filling volume. This stage marks the transition to a pathological condition, with diastolic dysfunction and a tendency towards decompensation.
Terminal stage: diastolic and systolic dysfunction → The dilated ventricle becomes less efficient, the myocardium undergoes fibrosis, and there is a reduction in ejection fraction with progression towards heart failure.
The electrocardiogram (ECG) may show signs of left ventricular hypertrophy, such as increased QRS complex voltage and leftward cardiac axis deviation. However, the diagnostic gold standard remains echocardiography, which allows assessment of myocardial thickness. Interventricular septum values greater than 10 mm are considered indicative of pathological hypertrophy, although they should be interpreted according to patient body size.
Left ventricular hypertrophy not only impairs ventricular function, but also leads to increased left atrial pressure. Over time, this results in left atrial dilation, with consequent alterations in atrial electrical architecture and a higher predisposition to supraventricular arrhythmias, including atrial fibrillation (AF).
AF in hypertensive patients represents 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: secondary to rupture of an atherosclerotic plaque and formation of coronary thrombi.
Chronic ischemic heart disease: characterized by progressive reduction in myocardial function due to prolonged ischemia.
If not properly treated, arterial hypertension may evolve into 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 atrial filling pressures. It presents with exertional dyspnea and pulmonary congestion.
Heart failure with reduced ejection fraction (HFrEF): the myocardium progressively weakens, reducing its contractile capacity and causing a decline in ejection fraction, with a high risk of overt cardiac decompensation.
Conclusion
Arterial hypertension is a primary risk factor for cardiovascular diseases, requiring constant monitoring and prompt treatment to prevent the progression of cardiac damage. Therapeutic management includes blood pressure control with antihypertensive drugs, reduction of myocardial overload, and prevention of ischemic and arrhythmic complications.
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