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Aims Cardiac resynchronization therapy (CRT) in heart failure is limited by many non-responders. This study explores whether degree of wasted left ventricular (LV) work identifies CRT responders. Methods and results Twenty-one patients who received CRT according to guidelines were studied before and after 8+3 months. By definition, segments that shorten in systole perform positive work, whereas segments that lengthen do negative work. Work was calculated from non-invasive LV pressure and strain by speckle tracking echocardiography. For each myocardial segment and for the entire LV, wasted work was calculated as negative work in percentage of positive work. LV wall motion score index (WMSI) was assessed by echocardiography. Response to CRT was defined as ≥15% reduction in end-systolic volume (ESV). Responder rate to CRT was 71%. In responders, wasted work for septum was 117+102%, indicating more negative than positive work, and decreased to 14+12% with CRT (P , 0.01). In the LV free wall, wasted work was 19+16% and showed no significant change. Global LV wasted work decreased from 39+21 to 17+7% with CRT (P , 0.01). In non-responders, there were no significant changes. In multiple linear regression analysis, septal wasted work and WMSI were the only significant predictors of ESV reduction (b ¼ 0.14, P ¼ 0.01; b ¼ 1.25, P ¼ 0.03). Septal wasted work together with WMSI showed an area under the curve of 0.86 (95% confidence interval 0.71-1.0) for CRT response prediction. Conclusion Wasted work in the septum together with WMSI was a strong predictor of response to CRT. This novel principle should be studied in future larger studies. [ABSTRACT FROM AUTHOR]

Left ventricular (LV) circumferential strain and rotation have been introduced as clinical markers of myocardial function. This study investigates how regional LV apical rotation and strain can be used in combination to assess function in the infarcted ventricle. In healthy subjects (n = 15) and patients with myocardial infarction (n = 23), LV apical segmental rotation and strain were measured from apical short-axis recordings by speckle tracking echocardiography (STE) and MRI tagging. Infarct extent was determined by late gadolinium enhancement MRI. To investigate mechanisms of changes in strain and rotation, we used a mathematical finite element simulation model of the LV. Mean apical rotation and strain by STE were lower in patients than in healthy subjects (9.0 ± 4.9 vs. 12.9 ± 3.5° and -13.9 ± 10.7 vs. -23.8 ± 2.3%, respectively, P < 0.05). In patients, regional strain was reduced in proportion to segmental infarct extent (r = 0.80, P < 0.0001). Regional rotation, however, was similar in the center of the infarct and in remote viable myocardium. Minimum and maximum rotations were found at the infarct borders: minimum rotation at the border zone opposite to the direction of apical rotation, and maximum rotation at the border zone in the direction of rotation. The simulation model reproduced the clinical findings and indicated that the dissociation between rotation and strain was caused by mechanical interactions between infarcted and viable myocardium. Systolic strain reflects regional myocardial function and infarct extent, whereas systolic rotation defines infarct borders in the LV apical region. Regional rotation, however, has limited ability to quantify regional myocardial dysfunction. [ABSTRACT FROM AUTHOR]

The curvilinearity of the atrial pressure-volume curve implies that atrial compliance decreases progressively with increasing left atrial (LA) pressure (LAP), We predicted that reduced LA compliance leads to more rapid deceleration of systolic pulmonary venous (PV) flow. With this rationale, we investigated whether the deceleration time (tdec) of PV systolic flow velocity reflects mean LAP. In eight patients during coronary surgery, before extracorporeal circulation, PV flow by ultrasonic transit time and invasive LAP were recorded during stepwise volume loading. The tdec was calculated using two methods: by drawing a tangent through peak deceleration and by drawing a line from peak systolic flow through the nadir between the systolic and early diastolic flow waves. LA compliance was calculated as the systolic PV flow integral divided by LAP increment. Volume loading increased mean LAP from 11 ± 3 to 20 ± 5 mmHg (P < 0.001) (n = 40), reduced LA compliance from 1.16 ± 0.42 to 0.72 ± 0.40 ml/mmHg (P < 0.004) (n = 40), and reduced tdec from 320 ± 50 to 170 ± 40 ms (P < 0.0005) (n = 40). Mean LAP correlated well with tdec (r = 0.84, P < 0.0005) (n = 40) and LA compliance (r = 0.79, P < 0.0005) (n = 40). Elevated LAP caused a decrease in LA compliance and therefore more rapid deceleration of systolic PV flow. The tdec has potential to become a semiquantitative marker of LAP and an index of LA passive elastic properties. [ABSTRACT FROM AUTHOR]

Left ventricular diastolic dysfunction is associated with slowing of LV relaxation and a decrease in LV chamber compliance. This impairment of function leads to changes in filling velocities as measured by pulsed wave Doppler echocardiography in the pulmonary veins and across the mitral valve, and in intraventricular flow propagation velocity as measured by color M-mode Doppler. This paper explores some of the physiology of LV filling in a clinical context. [ABSTRACT FROM AUTHOR]