Exercise and cardiovascular outcomes in hypertensive patients in relation to structure and function of left ventricular hypertrophy: the LIFE study.
BACKGROUND
Exercise lowers blood pressure and improves cardiovascular function, but little is known about whether exercise impacts cardiovascular morbidity and mortality independent of left ventricular hypertrophy (LVH) and LV geometry.


METHODS
Observational analysis of prospectively obtained echocardiographic data within the context of a randomized trial of antihypertensive treatment.


METHODS
A total of 937 hypertensive patients with ECG LVH were studied by echocardiography in the Losartan Intervention For Endpoint reduction in hypertension study. Baseline exercise status was categorized as sedentary (never exercise), intermediate (<or=30 min twice/week), or physically active (>30 min twice/week). During 4.8-year follow-up, 105 patients suffered the primary composite endpoint of myocardial infarction (MI), stroke, or cardiovascular death. MI occurred in 39, stroke in 60, and cardiovascular death in 33 patients.


RESULTS
Sedentary individuals (n = 212) had, compared with those physically active (n = 511), higher heart rate (P<0.001), weight (P<0.001), body surface area (P = 0.02), body mass index (P<0.001), LV mass (LVM, P = 0.04), LVM indexed for height or body surface area (P = 0.004); thicker ventricular septum (P = 0.012) and posterior wall (P = 0.016); and larger left atrium (P = 0.006). Systolic variables did not differ. In Cox regression analysis, physically active compared with sedentary patients had lower risk of primary composite endpoint [odds ratio (OR): 0.42, 95% confidence interval (CI): 0.26-0.68, P < 0.001], cardiovascular death (OR: 0.50, 95% CI: 0.22-0.1.10, NS), and stroke (OR: 0.26, 95% CI: 0.13-0.49, P < 0.001) without significant difference for MI (OR: 0.79, 95% CI: 0.35-1.75, NS) independent of systolic blood pressure, LVM index, or treatment.


CONCLUSIONS
In hypertensive patients with LVH, physically active patients had improved prognosis for cardiovascular endpoints, mortality, and stroke that was independent of LVM.
Boman
Kurt
K
Department of Medicine, Skellefteå County Hospital, Skellefteå, Sweden. kurt.boman@vll.se
Gerdts
Eva
E
Wachtell
Kristian
K
Dahlöf
Björn
B
Nieminen
Markku S
MS
Olofsson
Mona
M
Papademetriou
Vasilios
V
Devereux
Richard B
RB
D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure; D015444:Exercise; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000401:mortality / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology / Q000401:mortality / Q000503:physiopathology; D019808:Losartan / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000209:etiology / Q000401:mortality / Q000503:physiopathology / Q000517:prevention & control*; D016017:Odds Ratio; D016016:Proportional Hazards Models; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D020521:Stroke / Q000209:etiology / Q000401:mortality / Q000503:physiopathology / Q000517:prevention & control*; D016896:Treatment Outcome; D014463:Ultrasonography; D016277:Ventricular Function, Left
D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D019808:Losartan