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[Hypertensive cardiopathy. From arterial hypertension to congestive heart failure]
1Serviço de Medicina Interna do Hospital St. Maria, Lisboa.
Insights
High blood pressure (HBP) significantly increases the risk of chronic heart failure (CHF) by causing left ventricular hypertrophy (LVH). Preventing LVH progression and treating HBP are crucial for CHF prevention.
Area of Science:
- Cardiovascular Medicine
- Hypertension Research
- Heart Failure Pathophysiology
Context:
- Arterial hypertension (HBP) is a major cardiovascular risk factor, strongly linked to chronic heart failure (CHF).
- Hypertension contributes to 39-59% of CHF cases and is associated with coronary artery disease (CAD).
- HBP frequently leads to left ventricular hypertrophy (LVH), a key factor in heart failure development.
Purpose:
- To elucidate the pathophysiological links between HBP, LVH, and the progression to CHF.
- To explore the molecular and structural changes in the myocardium associated with HBP-induced cardiac dysfunction.
- To highlight potential therapeutic strategies for preventing CHF in hypertensive patients.
Summary:
- HBP causes LVH, characterized by cardiomyocyte hypertrophy, interstitial fibrosis, and coronary artery changes, leading to diastolic and systolic dysfunction.
- Progression to CHF involves increased microtubular structures, reduced sarcoplasmic reticulum Ca++ ATPase, and altered growth factor expression (TGF-β1).
- Myocardial apoptosis, induced by tumor necrosis factor-alpha, NO-synthase, and oxidative stress, further contributes to CHF progression.
Impact:
- Understanding these mechanisms is vital for developing targeted interventions to prevent CHF.
- Effective CHF prevention requires managing HBP, regressing LVH, and normalizing myocardial components.
- Therapeutic approaches may include renin-angiotensin system inhibitors and potentially gene therapy.
Abstract:
Arterial hypertension (HBP) is a very important cardiovascular risk factor. According to the data from the Framingham Study, 90% of the patients with chronic heart failure (CHF) have a clinical history of HBP, and the risk of developing CHF is 2 to 3 times greater in hypertensive persons. Studies of general population by multivariate analysis have shown that HBP is responsible for 39% of CHF cases in males and 59% in females. On the other hand, there is a significant relation between HBP and coronary artery disease (CAD), another very important cause of CHF. HBP very frequently originates left ventricular hypertrophy (LVH) and this is one of the most important links between HBP, myocardium ischaemia, CAD, and sudden death from arrhythmias, to which it can lead. Recent studies on left ventricle systolic function in hypertensive patients indicate that about 1/6 of HBP patients with LVH present systolic dysfunction. Even more frequently, diastolic function is prematurely deteriorated in HBP. In spite of the existence of a significant relation between the grade of LVH and the severity of this disfunction, it may be present even before LVH is detectable. The transition from LVH would be related to quantitative and qualitative changes in the three compartments of the myocardium: hypertrophy of cardiomyocytes with reinduction of fetal genetic program, reactive and cicatricial fibrosis of the interstice, and functional and structural changes of coronary arteries. These modifications will progressively increase, leading to LV dilation which seems to signal transition to heart failure. In recent papers the transition from LVH to CHF has been related to a marked increase in microtubular intracytoplasmic structure, the reduction of Ca++ ATPase concentration of the sarcoplasmic reticulum, and the increased myocardial expression of growth factor TGF beta 1, which influences interstitial fibrosis. In the same way, stimulation of apoptosis by myocardial expression of tumor necrosis factor alpha and the subquent increase in inducible NO-synthase and oxidative stress has been related to the progression for CHF. Prevention of CHF will not only consist in the treatment of HBP but, very probably, also in the prevention of regression of LVH, and normalization of myocardial components, as well as the correction of all the factors involved in CHF establishment. In accordance with form of treatment, we must give special emphasis to drugs interfering with the renin-angiotensin system and, possibly in the near future, to gene therapy.