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Contractile performance following regression of left ventricular hypertrophy in hypertensive patients
M M Ibrahim1, H Emile, M A Madkour
1Cardiac Department, Cairo University, Egypt.
Insights
Guanfacine effectively reduces left ventricular hypertrophy in hypertensive patients. This treatment improves cardiac structure without negatively impacting myocardial contractility, as measured by the end systolic stress-end systolic dimension relation.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Research
Background:
- Left ventricular hypertrophy (LVH) is a common complication of hypertension.
- Assessing myocardial contractility is crucial for understanding the effects of LVH regression.
Purpose of the Study:
- To evaluate the impact of guanfacine-induced LVH regression on myocardial contractility.
- To determine if decreased left ventricular mass affects intrinsic cardiac performance.
Main Methods:
- Utilized the end systolic stress-end systolic dimension (ESS-ESD) relation to assess contractility.
- Employed echocardiography to measure left ventricular dimensions and wall thickness before and after 10 weeks of guanfacine treatment.
- Infused sodium nitroprusside to modify left ventricular afterload during assessments.
Main Results:
- Guanfacine significantly reduced arterial pressure, wall thickness, and left ventricular mass (cross-sectional area).
- The ESS-ESD slope, indicating contractility, remained unchanged in patients with and without LVH and did not alter with decreased left ventricular mass.
Conclusions:
- Guanfacine effectively induces regression of left ventricular hypertrophy in hypertensive individuals.
- Regression of left ventricular mass does not impair the intrinsic contractile function of the left ventricle.
Abstract:
The left ventricular end systolic stress-end systolic dimension (ESS-ESD) relation was used to assess the effect of regression in left ventricular hypertrophy on myocardial contractility in 14 hypertensive patients (mean age 47 years) treated with guanfacine (a sympatholytic central alpha-adrenergic agonist) for 10 weeks. Echocardiography (M-mode under two-dimensional guidance) was used to determine left ventricular dimensions, posterior wall thickness (PWT) and septal thickness (ST) before and during the last week of therapy. Left ventricular mass (LVM) expressed as cross-sectional area (CSA) and meridianal wall stress at end systole were derived. Echocardiography was carried out at rest and during i.v. infusion of sodium nitroprusside to alter left ventricular afterload. A minimum of four systolic arterial pressure-ESD points were available for analysis and the value for the slope ESS-ESD was calculated for each patient. Guanfacine produced a significant decrease (P < 0.005) in arterial pressure, wall thickness and CSA. The linear ESS-ESD slope was similar in patients with and without left ventricular hypertrophy and did not change in the whole group or in four patients who had a decrease in CSA of > 10%. It is concluded that guanfacine can induce regression of left ventricular hypertrophy in hypertensive patients and that a decrease in LVM does not influence the intrinsic contractile performance of the left ventricular.