Left ventricular (LV) systolic wall strain is a new candidate for prognostic indicator of hypertensive heart failure. It remains unclear how underlying transmural structural remodeling corresponds to LV wall systolic deformation as hypertensive hypertrophy progresses. We fed 68 Dahl salt-sensitive rats a high-salt (hypertensive group) or low-salt diet (control group) from 6 weeks old. At 10, 14, and 18 weeks, pressure-volume relation, transmural distribution of LV fibrosis, and myocyte hypertrophy were evaluated. LV global longitudinal and circumferential strain was measured with speckle tracking echocardiography. Emax was preserved throughout the study period, whereas τ and end-diastolic pressure-volume relation progressively deteriorated from 14 weeks (diastolic dysfunction stage). Lung weight increased significantly at 18 weeks (decompensated stage). Histological percentage area fibrosis and collagen type I/III, myocyte hypertrophy, and α-myosin heavy chain isoform increased in the subendocardial layer at 14 weeks and progressed into the midlayer at 18 weeks. Longitudinal strain progressively deteriorated in the hypertensive group versus control group at 14 weeks (hypertensive group: -17±3%, control: -27±4%; P<0.001), and circumferential strain decreased at 18 weeks (hypertensive group: -17±2%, control: -27±3%; P=0.002). After adjustment for systolic wall stress, subendocardial percentage area fibrosis was selected as the independent determinant of longitudinal strain. This study showed that LV wall strain alternations were accompanied by fibrosis and myocyte hypertrophy from subendocardium to epicardium, and longitudinal strain related significantly to subendocardial layer fibrosis. Longitudinal strain could be a surrogate of subendocardial fibrotic changes and may be useful for risk stratification of hypertensive heart failure.

Diabetic microangiopathy and its accumulated effects significantly related to subclinical LV dysfunction are characterized by impaired longitudinal shortening.

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Introduction: Cardiac hypertrophy is an independent risk factor for sudden cardiac death from ventricular tachyarrhythmias (VT). Granulocyte colony-stimulating factor (G-CSF) has recently been reported to suppress VT after myocardial infarction by modulating the function of gap junctions between cardiomyocytes via maintaining Connexin-43 (Cx43). We hypothesized that the G-CSF could also regress an enhanced vulnerability to VT in the cardiac hypertrophy without ischemic fibrosis through regulating Cx43. Methods: Dahl salt-sensitive rats were maintained for a 6 week-period on a high-salt diet as left ventricular hypertrophy models (LVHs) and a low-salt diet as controls (CONs). After 3-time subcutaneous injection (50 μ g/kg) of G-CSF and vehicle, the inducibility of VT was evaluated by rapid ventricular burst pacing. The electrical pulses for the induction of VT were square waves with 6 ms width at 6 V and delivered at 25 Hz for 30 sec. White blood cell was counted to confirm a response to the G-CSF treatment. Expression levels of phosphorylated and total Cx43 in the rat ventricles were analyzed by immunoblotting. Results: The LVHs showed apparent cardiac hypertrophy without pathological fibrotic changes. The G-CSF reduced the inducibility of VT compared to the vehicle in the LVHs (11 % vs. 63 %, p=0.04). Furthermore, the G-CSF eliminated the inducibility of VT in the CONs, although a difference in the inducibility of VT between with and without the G-CSF treatment did not reach statistical significance in the CONs (0 % vs. 33 %, p=0.60). White blood cell count in one microliter of blood was elevated by the G-CSF treatment in both LVHs (15083±4397 vs. 6976±1308, p<0.01) and CONs (19370±1174 vs. 7700±2335, p<0.01). The G-CSF increased phosphorylated Cx43 levels compared to the vehicle in both LVHs (1.4-fold vs. 1.2-fold, p<0.01) and CONs (1.4-fold vs. 1.0-fold, p=0.04), whereas the G-CSF did not affect total Cx43 levels in all groups. Conclusion: We demonstrated that the G-CSF administration ameliorated the electrophysiological stability in the rat model of cardiac hypertrophy by modulating the function of gap junctions through accelerating phosphorylation of Cx43.