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Impairment of cardiac function in hypertensive patients with Type 2 diabetes: a LIFE study
P Hildebrandt1, K Wachtell, B Dahlöf
1Frederiksberg University Hospital, Frederiksberg, Denmark. ph@fh.hosp.dk
Insights
Type 2 diabetes impairs cardiac function in hypertensive patients with left ventricular hypertrophy, independent of increased heart muscle mass. Diabetes itself adversely affects both systolic and diastolic heart function.
Area of Science:
- Cardiology
- Diabetology
- Hypertension Research
Background:
- Type 2 diabetes and hypertension commonly coexist.
- Hypertension leads to increased left ventricular (LV) mass and impaired cardiac function.
- The independent contribution of diabetes to cardiac dysfunction in hypertensive patients with LV hypertrophy is unclear.
Purpose of the Study:
- To compare LV function between diabetic and non-diabetic hypertensive patients with electrocardiographic LV hypertrophy.
- To determine if impaired cardiac function is solely due to LV hypertrophy or independently related to diabetes.
Main Methods:
- Analysis of echocardiograms from 937 patients in the LIFE echocardiographic substudy.
- Centralized evaluation of LV mass, systolic, and diastolic LV function.
- Comparison between 105 diabetic patients and non-diabetic hypertensive patients.
Main Results:
- Left ventricular mass was similar between diabetic and non-diabetic groups.
- Diabetic patients showed reduced endocardial systolic function (LV ejection fraction) and impaired midwall systolic function.
- Diastolic LV filling was impaired, and arterial stiffness was increased in diabetic patients.
Conclusions:
- Cardiac systolic and diastolic function are impaired in hypertensive patients with LV hypertrophy and diabetes.
- These impairments are independent of LV mass.
- The findings suggest adverse effects of diabetes per se on cardiac function.
Aims:
Type 2 diabetic patients with hypertension have an increased left ventricular (LV) mass and impaired cardiac function compared to hypertensive patients without diabetes. However, it is unknown if the impaired cardiac function can be explained solely by LV hypertrophy, or is independently related to diabetes. The aim of the present study was to compare LV function between diabetic and non-diabetic hypertensive patients with electrocardiographic LV hypertrophy.
Methods:
In 937 patients participating in the LIFE echocardiographic substudy, all echocardiograms were centrally evaluated by a core reading centre measuring LV mass, systolic and diastolic LV function. Known diabetes was present in 105 patients.
Results:
Left ventricular mass was similar in diabetic and non-diabetic patients. Endocardial systolic LV function, estimated by LV ejection fraction, was reduced and indices of midwall systolic LV function were impaired in the diabetic patients. Diastolic LV filling pattern was impaired and arterial stiffness, measured by pulse pressure/stroke index, was increased in diabetic patients.
Conclusions:
Systolic and diastolic LV function in hypertensive patients with electrocardiographic LV hypertrophy and diabetes are impaired independent of LV mass, most likely reflecting the adverse effects of diabetes per se.
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