Coronary flow reserve in the newborn lamb: an intracoronary Doppler guide wire study.

Recent studies indicate a severely reduced coronary flow reserve (CFR) in neonates with congenital heart disease. The significance of these studies remains debatable, as the ability of the anatomically normal neonatal heart to increase coronary flow is currently unknown. This study was designed to establish normal values for CFR in newborns after administration of adenosine [pharmacologic CFR (pCFR)] and as induced by acute hypoxemia (reactive CFR). Thirteen mechanically ventilated newborn lambs were studied. Coronary flow velocities were measured in the proximal left anterior descending coronary artery before and after adenosine injection (140 and 280 microg/kg i.v.) using an intracoronary 0.014-in Doppler flow-wire. Measurements were made at normal oxygen saturation (SaO(2)) and during progressive hypoxemia induced by lowering the fraction of inspired oxygen. CFR was defined as the ratio of hyperemic to basal average peak flow velocity. In a hemodynamically stable situation with normal SaO(2), pCFR was 3.0 +/- 0.5. pCFR decreased with increasing hypoxemia. Regression analysis showed a linear relation between SaO(2) and pCFR (R = 0.86, p < 0.0001). Reactive CFR obtained at severe hypoxemia (Sao(2) <30%) was 4.2 +/- 0.8, and no significant further increase in coronary flow velocity occurred by administration of adenosine. Newborn lambs have a similar capacity to increase coronary flow in response to both pharmacologic and reactive stimuli as older subjects. Administration of adenosine does not reveal the full capacity of the newborn coronary circulation to increase flow, however, as the flow increase caused by severe hypoxemia is significantly more pronounced.

Acute Chlamydia pneumoniae infection causes coronary endothelial dysfunction in pigs.

BACKGROUND: Coronary endothelial dysfunction contributes to the pathogenesis of acute coronary syndromes (ACSs). Acute Chlamydia pneumoniae infection has been epidemiologically associated with ACS. In this study, we investigated whether acute C. pneumoniae infection could alter the endothelial vasomotor function of porcine coronary vessels. METHODS AND RESULTS: Twenty pigs, 7-9 kg in weight, were inoculated intratracheally with C. pneumoniae (n=12) or saline (n=8), and investigated at 3 days (five infected/four non-infected) and 2 weeks (5+2 infected/four non-infected) after inoculation. The endothelium-dependent reactivity of coronary microcirculation was assessed at both time points by measuring peak coronary flow velocity (CFV) in response to bradykinin, before and after infusions with glutathione, an antioxidant, and L-arginine, a substrate for nitric oxide synthase (NOS). CFV after bradykinin was significantly decreased in infected animals at both time points. At 2 weeks, both glutathione and L-arginine significantly improved CFV after bradykinin. CFV after sodium nitroprusside (SNP) was similar in both groups. At 3 days, the relaxation responses of bradykinin-induced pre-contracted left anterior descending (LAD) coronary rings to bradykinin were significantly less in infected animals. N(G)-nitro-L-arginine-methyl-ester, an NOS inhibitor, had significantly greater inhibitory effect on bradykinin-induced relaxation in infected animals. Plasma nitrate-nitrite and fibrinogen, and NOS activity from LAD coronary samples were significantly increased in infected animals. CONCLUSION: Acute C. pneumoniae infection causes endothelial dysfunction of both resistance and epicardial coronary vessels, and favours a pro-coagulant status. These effects could in part account for the epidemiologically suggested association between acute infection and ACS.

Normal coronary flow reserve after arterial switch operation for transposition of the great arteries: an intracoronary Doppler guidewire study.

BACKGROUND: Recent studies performed with positron emission tomography have suggested that coronary flow reserve (CFR) is moderately to severely reduced after the arterial switch operation (ASO). These findings are of great concern but have not been confirmed by other methods. METHODS AND RESULTS: Eleven symptom-free children were studied between 4 and 11 (median 6.0) years after the ASO. Flow velocity in the left anterior descending (LAD) and right coronary arteries (RCA) was measured with a 0.014-inch Doppler FloWire (Cardiometrics) before and after intracoronary injection of adenosine (0.5 microg/kg) and nitroglycerin (5 microg/kg). CFR was defined as the ratio of hyperemic to basal average peak velocity (APV). The median (range) CFR in the LAD was 3.7 (3.0 to 4.8) and 3.4 (2.9 to 4.8) in the RCA. The increase in APV after intracoronary injection of nitroglycerin was 300% (240% to 420%) in the LAD and 260% (190% to 460%) in the RCA. APV at rest was 15.0 (14.0 to 21.0) cm/s in the LAD and 16.0 (9.6 to 30.0) cm/s in the RCA. A linear relation was found between right ventricular systolic pressure and resting APV in the RCA (r=0.77, P=0.0056), and between resting APV and CFR (r=-0.61, P<0.05) in the RCA. CONCLUSIONS: The CFR and coronary vasoreactivity to nitroglycerin in children treated for transposition of the great arteries with the ASO was within normal limits. Increased right ventricular pressure and myocardial hypertrophy can cause increased resting coronary flow velocity in the RCA and affect CFR negatively.

Collateral flow in coarctation of the aorta with magnetic resonance velocity mapping: correlation to morphological imaging of collateral vessels.

PURPOSE: To correlate quantification of collateral flow in aortic coarctation with the morphological visualization of the collateral vessels and to compare different approaches to measurement of collateral flow. MATERIALS AND METHODS: Thirteen children with coarctation were examined with T1-weighted spin-echo (T1-W SE) imaging and 3D contrast-enhanced magnetic resonance angiography (MRA). MR velocity mapping was performed at four levels in the descending aorta. RESULTS: The flow immediately above and below the coarctation did not differ significantly. Measuring within the coarctation resulted in flow overestimation. The increase of flow from proximal to distal aorta was 12 +/- 21% in patients with no or uncertain collaterals and 69 +/- 55% in patients with pronounced collaterals. Spin-echo images and MRA were comparable in visualizing collateral vessels. The visual estimation of collaterals correlated reasonably well with flow quantification MR velocity mapping. CONCLUSION: Collateral flow assessment with MR velocity mapping is an accurate technique for evaluating the hemodynamic importance of a coarctation and is recommended if abundant collaterals are not visualized with spin echo or MRA.