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Regression of cardiovascular structural changes by antihypertensive treatment. Functional consequences and time
Insights
Antihypertensive treatment reduces left ventricular (LV) wall thickness and improves cardiac function in two phases. Initially, LV mass decreases, followed by improved LV compliance and reduced vascular resistance.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Antihypertensive treatment is known to affect cardiac structure and function.
- Left ventricular (LV) mass and function are key indicators of cardiovascular health.
Purpose of the Study:
- To investigate the temporal changes in left ventricular (LV) mass, function, and peripheral resistance during antihypertensive treatment.
- To elucidate the mechanisms underlying these changes in different phases of treatment.
Main Methods:
- Echocardiographic studies were utilized to assess LV wall thickness, LV end-diastolic diameter, and LV function.
- Hemodynamic parameters including cardiac output and total peripheral resistance were analyzed.
Main Results:
- Treatment initially reduced LV mass and cardiac output, with no change in peripheral resistance.
- A second phase showed constant LV mass but increased cardiac output and decreased peripheral resistance.
- Increased LV compliance and reversal of vascular changes were observed.
Conclusions:
- Antihypertensive therapy induces distinct early and late phases of cardiovascular adaptation.
- Improved LV compliance and vascular remodeling contribute to favorable hemodynamic changes during long-term treatment.
Abstract:
Echocardiographic studies have shown a decrease in left ventricular (LV) wall thickness and an improvement in LV function during antihypertensive treatment. A reduction in LV mass parallels the reduction in LV wall thickness during the first year of antihypertensive treatment, but thereafter favorable changes in LV wall thickness, cardiac output, and total peripheral resistance may be recorded in spite of a constant LV mass. The reason for this is that LV mass is defined by LV wall thickness and LV end-diastolic diameter, and that LV mass may stay unchanged if LV wall thickness decreases when LV diameter increases. This pattern of change is to be expected since LV distensibility and, hence, LV end-diastolic diameter may increase when LV wall thickness decreases. The effect of treatment may thus be divided into two main phases--an initial phase with a reduction in LV mass and a reduction in cardiac output and no change in total peripheral resistance--and a second phase with a constant LV mass but an increase in cardiac output to the pretreatment level again and a concomitant decrease in total peripheral resistance. The increase in stroke volume and cardiac output during this second phase of treatment is mainly dependent on an increase in end-diastolic volume, most likely explained by improved LV compliance when LV wall thickness decreases. The concomitant decrease in total peripheral resistance is mainly explained by reversal of structural vascular changes.(ABSTRACT TRUNCATED AT 250 WORDS)