Myocardial mechano-energetic efficiency in hypertensive adults

Myocardial mechanical efficiency can be measured as the ratio between systolic work and energy consumption. We evaluated the relation between myocardial mechanical efficiency and left ventricular (LV) mass in untreated hypertensive patients.

Myocardial work was estimated in 256 normotensive (35 +/- 12 years) and 306 hypertensive patients (47 +/- 10 years) with normal ejection fraction, as stroke work in gram-meters (stroke work = BPs x SV x 0.0144, where BPs is systolic blood pressure, SV is echocardiographic stroke volume). Myocardial O2 consumption was estimated as the product of heart rate (HR) x BPs (eMVO2). Myocardial mechanical efficiency was estimated as the ratio of stroke work/eMVO2, which can be simplified and expressed as ml/s.

LV mass was greater in hypertensive than in normotensive patients (46 +/- 13 vs. 38 +/- 11 g/m2.7, P < 0.0001), but myocardial mechanical efficiency was identical (85 +/- 23 vs. 86 +/- 26 ml/s). Relations between myocardial mechanical efficiency and LV mass were close (both P < 0.0001), but more scattered among hypertensive patients because of 56 patients exhibiting low myocardial mechanical efficiency relative to the magnitude of LV mass. At comparable age and body size, these patients had higher HR, BPs, and pulse pressure than those with normal myocardial mechanical efficiency (all P < 0.001). After adjusting for age and sex, hypertensive patients with low myocardial mechanical efficiency showed greater relative wall thickness and lower ejection fraction and midwall shortening than those with normal myocardial mechanical efficiency (all P < 0.001). Low myocardial mechanical efficiency was also associated with inappropriately high LV mass (P < 0.0001).

In some hypertensive patients the left ventricle works inefficiently with a high energy wasting, at the same level of LV mass as hypertensive patients with normal myocardial mechanical efficiency. Those patients feature a high cardiovascular risk phenotype, with concentric LV geometry, systolic dysfunction, and indirect signs of more severe vascular impairment.