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Regression of structural cardiovascular changes by antihypertensive therapy
Insights
Structural vascular changes in hypertension are reversible with long-term blood pressure reduction. However, complete normalization is difficult due to fibrosis and drug effects, impacting antihypertensive therapy effectiveness.
Area of Science:
- Cardiovascular Medicine
- Hypertension Research
- Vascular Biology
Background:
- Hypertension is associated with structural arteriolar changes, primarily smooth muscle cell hypertrophy.
- These vascular changes can be a primary phenomenon or secondary to elevated arterial pressure.
- Structural arteriolar changes are observed in both animal models and human patients with hypertension.
Purpose of the Study:
- To investigate the reversibility of structural vascular changes in hypertension.
- To explore factors influencing the normalization of arteriolar media in response to antihypertensive therapy.
- To compare the efficacy of different antihypertensive drug classes in reversing vascular remodeling.
Main Methods:
- Review of studies on hypertensive animal models and patients.
- Analysis of vascular changes in response to chronic antihypertensive therapy.
- Comparison of antihypertensive drugs with and without vasodilating properties.
Main Results:
- Structural arteriolar changes are reversible with sustained reduction in arterial pressure in animal models and some human vascular beds.
- Complete normalization is often not achieved due to inadequate pressure reduction and induced fibrosis.
- Antihypertensive drugs with vasodilating actions appear more effective in reversing structural changes than non-vasodilating agents.
Conclusions:
- Long-term blood pressure reduction can lead to regression of hypertensive vascular changes.
- Fibrosis in the arteriolar media may limit the complete reversibility of structural changes.
- Vasodilating antihypertensive drugs may offer additional benefits in vascular remodeling beyond blood pressure lowering.
Abstract:
Structural vascular changes, consisting mainly of smooth muscle cell hypertrophy of the arterioles, have been found in various hypertensive animal models as well as in hypertensive patients. Although such changes may be to some extent a primary phenomenon in primary or essential hypertension, there is ample proof that an elevation in arterial pressure over a period of time will cause hyperplasia of the media in the resistance vessels; thus, this change is secondary to the rise in pressure. Studies in various animal models have shown that such structural arteriolar changes are reversible if a long-term reduction in arterial pressure can be obtained. In hypertensive patients reversibility of such changes has been demonstrated in some vascular beds as a result of chronic antihypertensive therapy. However, no complete "normalization" has ever been shown, probably because of inadequate reduction of arterial pressure and perhaps also because long-standing hypertension induces fibrosis of the arteriolar media, which is less likely to be positively affected by a lowering of blood pressure. In humans, some vascular beds, for example, the muscle vessel bed of the calves, appear to be less suitable for the demonstration of regression of structural changes. This could be due to erect posture, which increases the transmural pressure in these vessels, since the effect of gravity is added to the intravascular pressure. Finally, it is conceivable that effects other than the reduction in arterial pressure could play a role. Thus, antihypertensive drugs with a vasodilating action appear to be more effective in reducing structural vascular changes than drugs that do not have a vasodilating effect, even if an identical degree of blood pressure reduction is obtained.(ABSTRACT TRUNCATED AT 250 WORDS)