A systolic long-axis peak velocity of <11 cm/s at the lateral tricuspid annulus most accurately detects moderately impaired RVEF as obtained by MRI; severely reduced RVEF ≤30% is best detected by RV MPI at a value of >0.50.

ECP appears to be effective in promoting coronary collateral growth. The extent of collateral function improvement is related to the amount of improvement in the systemic endothelial function.

Background-The efficacy of granulocyte colony-stimulating factor (G-CSF) for coronary collateral growth promotion and thus impending myocardial salvage has not been studied so far, to our best knowledge. Methods and Results-In 52 patients with chronic stable coronary artery disease, age 62Ϯ11 years, the effect on a marker of myocardial infarct size (ECG ST segment elevation) and on quantitative collateral function during a 1-minute coronary balloon occlusion was tested in a randomized, placebo-controlled, double-blind fashion. The study protocol before coronary intervention consisted of occlusive surface and intracoronary lead ECG recording as well as collateral flow index (CFI, no unit) measurement in a stenotic and a Ն1 normal coronary artery before and after a 2-week period with subcutaneous G-CSF (10 g/kg; nϭ26) or placebo (nϭ26). The CFI was determined by simultaneous measurement of mean aortic, distal coronary occlusive, and central venous pressure. The ECG ST segment elevation Ͼ0.1 mV disappeared significantly more often in response to G-CSF (11/53 vessels; 21%) than to placebo (0/55 vessels; Pϭ0.0005), and simultaneously, CFI changed from 0.121Ϯ0.087 at baseline to 0.166Ϯ0.086 at follow-up in the G-CSF group, and from 0.152Ϯ0.082 to 0.131Ϯ0.071 in the placebo group (PϽ0.0001 for interaction of treatment and time). The absolute change in CFI from baseline to follow-up amounted to ϩ0.049Ϯ0.062 in the G-CSF group and to Ϫ0.010Ϯ0.060 in the placebo group (PϽ0.0001). Conclusions-Subcutaneous

Background: Coronary collaterals protect myocardium jeopardized by coronary artery disease (CAD). Promotion of collateral circulation is desirable before myocardial damage occurs. Therefore, determinants of collateral preformation in patients without CAD should be elucidated. Methods: In 106 patients undergoing coronary angiography who were free of coronary stenoses, a total of 39 clinical test variables were collected. The coronary collateral flow index (CFI) was measured. Stepwise multiple linear regression analysis was performed after choosing a restricted number of candidates emerging from univariate testing. Separate multiple regression analyses were performed in patients with and without beta-blocker therapy. Results: Nine parameters were found to be possible determinants of CFI by univariate analysis: arterial hypertension (aHT), dyslipidemia, statins, diuretics, age, height, heart rate (HR), pulse pressure amplitude, and left ventricular end-diastolic pressure (LVEDP). After multiple regression analysis, a low HR, absence of aHT, and elevated LVEDP were significantly related to CFI (F = 5.31, p = 0.002, adjusted r² = 0.12). In patients without beta-blockers, a low HR and absence of aHT were independent predictors of CFI (F = 8.03, p < 0.001, n = 50, adjusted r² = 0.30). Conclusions: A low HR and absence of aHT are both related to collateral preformation in humans. We suppose that bradycardia favors fluid shear stress in coronary arteries, thus triggering collateral growth.

NCT01039389.