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Left Ventricular Longitudinal Strain as a Marker for Point of No Return in Hypertensive Heart Failure Treatment
Tomoko Ishizu1, Yoshihiro Seo2, Mikiko Namekawa3
1Department of Clinical Laboratory Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Insights
Early intervention with angiotensin-converting enzyme inhibitors (ACE-I) can prevent heart failure in hypertensive rats. Treatment before significant left ventricular strain or ejection fraction decline is key to avoiding irreversible cardiac remodeling.
Area of Science:
- Cardiology
- Hypertension Research
- Animal Models
Background:
- No current therapies improve prognosis for heart failure with preserved ejection fraction (HFpEF).
- A "point of no return" may exist in hypertensive HF, potentially linked to left ventricular (LV) strain.
- This study investigates early ACE-I treatment based on myocardial strain imaging.
Purpose of the Study:
- To determine if early intervention with an angiotensin-converting enzyme inhibitor (ACE-I) can prevent hypertensive heart failure.
- To identify the "point of no return" for myocardial remodeling in hypertensive heart failure using strain imaging.
- To evaluate the efficacy of ACE-I initiated at different stages of cardiac dysfunction in an animal model.
Main Methods:
- Thirty-two male Dahl salt-sensitive rats were divided into six groups, including low-salt and high-salt controls.
- ACE-I treatment was initiated at different time points: early (6 weeks), after longitudinal strain (LS) impairment (> -21%), after circumferential strain (CS) impairment (> -18%), or after ejection fraction (EF) decline (< 55%).
- Rats were sacrificed at 23 weeks for LV and lung weight measurements and pathological analysis.
Main Results:
- Early ACE-I treatment and treatment after LS impairment prevented increases in lung and LV weights, similar to low-salt controls.
- Subendocardial fibrosis was significantly reduced in the early and LS groups (<3%) compared to high-salt, EF, and CS groups (>6%).
- Echocardiography showed LS improvement in the LS group, but no significant differences in CS or EF were observed in the CS and EF groups, respectively.
Conclusions:
- Heart failure-related lung congestion was prevented by administering ACE-I soon after LS impairment.
- Early ACE-I treatment suppressed cardiac hypertrophy and fibrosis, indicating a potential point of no return after LS but before CS impairment.
- These findings suggest that targeting myocardial strain early is crucial for preventing irreversible hypertensive heart failure.
Background:
There are currently no therapies that can improve prognosis in cases of heart failure (HF) with preserved ejection fraction (EF). We hypothesized that there is a point of no return after which no response to treatment is noted and that for the prevention of hypertensive HF this point may be determined by left ventricle (LV) strain, in the prevention of hypertensive HF. Here an angiotensin-converting enzyme inhibitor (ACE-I) was initiated based on myocardial strain imaging and its effects were determined in an animal model.
Methods:
Thirty-two male Dahl salt-sensitive rats, age 6 weeks, were divided into six experimental groups and compared with low-salt (n = 8) and high-salt control groups (n = 8). In the early treatment group, ACE-I was administered from the age of 6 weeks (n = 4); in the longitudinal strain (LS) group, at 10-12 weeks when LS impairment was >-21% (n = 4); in the circumferential strain (CS) group, at 16-18 weeks when CS impairment was >-18% (n = 4); and in the EF group, at 20 weeks when EF was <55% (n = 4). Subsequently, all rats were sacrificed at 23 weeks age, the LV and lung weight were measured, and pathologic analyses were performed.
Results:
At 23 weeks of age, the lung and LV weights increased in the high-salt control, EF, and CS groups, whereas the lung and LV weights in the LS and early groups were similar to those in the low-salt control group. The percentage of area of subendocardial fibrosis was >6% in the high-salt control, EF, and CS groups and <3% in the LS, early, and low-salt groups. Serial echocardiography demonstrated LS improvement in the LS group; however, the CS and EF groups showed no differences.
Conclusions:
Heart failure-related lung congestion was prevented when ACE-I was administered soon after LS impairment, accompanied by suppression of cardiac hypertrophy and fibrosis, thereby suggesting that the point of no return of myocardial remodeling due to hypertension was present after LS but before CS impairment.
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