Left Ventricular Wall Stress–Mass–Heart Rate Product and Cardiovascular Events in Treated Hypertensive Patients

Abstract

Abstract-In the Losartan Intervention for End Point Reduction in Hypertension (LIFE) study, 4.8 years' losartan-versus atenolol-based antihypertensive treatment reduced left ventricular hypertrophy and cardiovascular end points, including cardiovascular death and stroke. However, there was no difference in myocardial infarction (MI), possibly related to greater reduction in myocardial oxygen demand by atenolol-based treatment. Myocardial oxygen demand was assessed indirectly by the left ventricular mass×wall stress×heart rate (triple product) in 905 LIFE participants. The triple product was included as time-varying covariate in Cox models assessing predictors of the LIFE primary composite end point (cardiovascular death, MI, or stroke), its individual components, and all-cause mortality. At baseline, the triple product in both treatment groups was, compared with normal adults, elevated in 70% of patients. During randomized treatment, the triple product was reduced more by atenolol, with prevalences of elevated triple product of 39% versus 51% on losartan (both P≤0.001). In Cox regression analyses adjusting for age, smoking, diabetes mellitus, and prior stroke, MI, and heart failure, 1 SD lower triple product was associated with 23% (95% confidence interval 13%-32%) fewer composite end points, 31% (18%-41%) less cardiovascular mortality, 30% (15%-41%) lower MI, and 22% (11%-33%) lower all-cause mortality (all P≤0.001), without association with stroke (P=0.34). Although losartan-based therapy reduced ventricular mass more, greater heart rate reduction with atenolol resulted in larger reduction of the triple product. Lower triple product during antihypertensive treatment was strongly, independently associated with lower rates of the LIFE primary composite end point, cardiovascular death, and MI, but not stroke. (Hypertension. 2015;66:945-953.

Surrogates for myocardial power and power efficiency in patients with aortic valve disease

“…The study follows previous research, which found increased LV myocardial oxygen demand (MVO 2 ) in hypertensive patients with LV hypertrophy 34 . The MVO 2 is determined mainly by three factors: heart rate, velocity of contraction and systolic wall tension together with the myocardial mass 35 .…”

Depressed Myocardial Energetic Efficiency Increases Risk of Incident Heart Failure: The Strong Heart Study

“…In our analysis, we provided an estimation of myocardial energetic efficiency using a very simple method on the basis of a simple assumption, which has been already used in different circumstances [5,18], i.e., that MVO2 consumption mainly depends on developed pressure and frequency of contraction. More complex models of estimating myocardial oxygen consumption have been proposed, with strong rationale, but are likely less suitable for a clinical use [21].…”

Indonesian herbal medicine prevents hypertension-induced left ventricular hypertrophy by diminishing NADPH oxidase-dependent oxidative stress

“…The result of our study demonstrated that CJID treatment prevented cardiac hypertrophy remodeling in SHRs. It has been determined that the response of increasing BP in the chronic hypertension, lead structural and functional changes specifically [ 10 ]. Our hypertensive rat model was characterized by left cardiac remodeling.…”

“…Indeed, recent studies have shown that LVH can increase cardiac-related death [ 9 ]. Therefore, the improvement of cardiac performance can be reached by inhibition of LVH independently of other risk factors [ 10 ].…”