No abstract

LEFT VENTRICULAR HYPERTROPHY (LVH) is an adaptive response to physiologic or pathologic stimuli and distinguishing between the two has obvious clinical implications. However, asymmetric septal hypertrophy and preserved cardiac function are noted in early stages in both cases. We characterized the early anatomic and functional changes in a mouse model of physiologic and pathologic stress using serial echocardiography-based morphometry and tissue velocity imaging. Weight-matched CF-1 male mice were separated into CONTROLS (n=10), treadmill EXERCISE 1 hour daily x 5 days/week (n=7) and transverse aortic constriction (TAC, n=7). Hypertrophy was noted first in the LV basal septum compared to other segments in EXERCİSE (0.84±0.02 vs. 0.79±0.03 mm, p=0.03) and TAC (0.86±0.05 vs. 0.77±0.04 mm, p=0.02) at 4 and 3 weeks, respectively. At 8 weeks, eccentric LVH was noted in EXERCISE and concentric LVH in TAC. Septal E/E' ratio increased in TAC (32.6±3.7 vs. 37±6.2, p=0.002) compared with the CONTROLS and EXERCISE (32.3±5.2 vs. 32.8±3.8 and 31.2±4.9 vs. 28.2±5.0, respectively, non-significant for both). Septal s' decreased in TAC (21±3.6 vs. 17±4.2 cm/s, p=0.04) but increased in EXERCISE (19.6±4.1 vs. 29.2±2.3 cm/s, p=0.001) and was unchanged in CONTROLS (20.1±4.2 vs. 20.9±5.1 cm/s, non-significant). Despite similar asymmetric septal hypertrophy and normal global function during the first 2-4 weeks of pathologic and physiologic stress, there is an early reduction in systolic tissue velocity in pathologic but preserved in physiologic hypertrophy. Tissue velocities may help adjudicate between these 2 states when there are no overt anatomic or functional differences.

Excessive sympathetic activity and stress-induced left ventricular (LV) hypercontractility have been described in hypertensive LV hypertrophy. Recent quantitative data have shown that hypertensive LV hypertrophy is associated with preserved global LV function. However, progression of uncontrolled hypertension have detrimental effects on both the ejection fraction (EF) and LV contractile response to stress. Hypertensive LV hypertrophy has some common characteristics, including preserved global LV systolic function and LV volume with heart failure with preserved EF (HFPEF), which makes it difficult to differentiate between the two conditions at rest. Studies suggest that adopting an efficient antihypertensive therapy regimen may positively effect on the LV contractile capability in patients with long-standing hypertension. Evaluation of quantitative LV contractility under stress may be beneficial to differentiate between the hypertensive LV hypertrophy and HFPEF. It may also assist in developing a more effective modality in medical management of patients with hypertensive heart disease.

Anatomic characteristics specific to HCM hearts contribute to lower correlations between MBF/MFR values obtained by PMod and QPET, compared with non-HCM patients. These differences indicate that PMod and QPET cannot be used interchangeably for MBF/MFR analyses in HCM patients.