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Objective: To evaluate the performance of dual source CT coronary angiography (DSCT-CA) in the detection of in-stent restenosis (⩾50% luminal narrowing) in symptomatic patients referred for conventional angiography (CA). Design/patients: 100 patients (78 males, age 62 (SD 10)) with chest pain were prospectively evaluated after coronary stenting. DSCT-CA was performed before CA. Setting: Many patients undergo coronary artery stenting; availability of a non-invasive modality to detect in-stent restenosis would be desirable. Results: Average heart rate (HA) was 67 (SD 12) (range 46-106) bpm. There were 178 stented lesions. The interval between stenting and inclusion in the study was 35 (SD 41) (range 3-140) months. 39/100 (39%) patients had angiographically proven restenosis. Sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of DSCT-CA, calculated in all stents, were 94%, 92%, 77% and 98%, respectively. Diagnostic performance at HA <70 bpm (n = 69; mean 58 bpm) was similar to that at HA ⩾70 bpm (n = 31; mean 78 bpm); diagnostic performance in single stents (n = 95) was similar to that in overlapping stents and bifurcations (n = 83). In stents ⩾3.5 mm (n = 78), sensitivity, specificity, PPV, NPV were 100%; in 3 mm stents (n = 59), sensitivity and NPV were 100%, specificity 97%, PPV 91%; in stents ⩽2.75 mm (n = 41), sensitivity was 84%, specificity 64%, PPV 52%, NPV 90%. Nine stents ⩽ 2.75 mm were uninterpretable. Specificity of DSCT-CA in stents ⩾3.5 mm was significantly higher than in stents ⩽2.75 mm (OR = 6.14; 99%Cl: 1.52 to 9.79). Conclusion: DSCT-CA performs well in the detection of in-stent restenosis. Although DSCT-CA leads to frequent false positive findings in smaller stents (⩽ 2.75 mm), it reliably rules out in-stent restenosis irrespective of stent size. [ABSTRACT FROM AUTHOR]

Objective: To determine whether inhaled NO (iNO) can reduce pulmonary vascular resistance in adults with congenital heart disease and obstructive pulmonary hypertension or Eisenmenger syndrome.Design: 23 patients received graded doses of iNO. Pulmonary and systemic haemodynamic variables and circulating cyclic guanosine monophosphate (cGMP) concentrations were measured at baseline and after 20 and 80 ppm iNO. Patients were considered responders when total pulmonary resistance was reduced by at least 20%, and rebound was defined as a greater than 10% increase in total pulmonary resistance upon withdrawal from iNO.Results: In response to 20 ppm iNO, total pulmonary resistance decreased in four patients (18%, 95% confidence interval (CI), 2% to 34%), while in response to 80 ppm iNO it decreased in six patients (29%, 95% CI 10% to 38%). Systemic blood pressure did not change. Withdrawal resulted in rebound in three patients (16%, 95% CI 0% to 32%) after cessation of 20 ppm iNO, and in six patients (35%, 95% CI 12% to 58%) after cessation of 80 ppm iNO. Patients with predominant right to left shunting did not respond. In all patients cGMP increased from (mean (SD)) 28 (13) micromol/l at baseline to 55 (30) and 78 (44) micromol/l after 20 and 80 ppm iNO (p < 0.05 v baseline).Conclusions: NO inhalation is safe and is associated with a dose dependent increase in circulating cGMP concentrations. Pulmonary vasodilatation in response to iNO was observed in 29% of patients and was influenced by baseline pulmonary haemodynamics. Responsiveness to acute iNO may identify patients with advanced obstructive pulmonary hypertension and Eisenmenger syndrome who could benefit from sustained vasodilator treatment. [ABSTRACT FROM AUTHOR]

Williams syndrome is a complex syndrome comprising developmental abnormalities, craniofacial dysmorphic features, and cardiac anomalies. The most common cardiac anomaly is supravalvular aortic stenosis. We report a case of a 6-year-old girl with Williams syndrome who presented with decompensated heart failure due to ischemic cardiomyopathy. Her only significant cardiac anomaly was severe stenosis of the left main coronary artery. She subsequently died despite surgical revascularization. Isolated coronary anomalies are rare in Williams syndrome but should be considered especially in the presence of heart failure or ischemia. [ABSTRACT FROM AUTHOR]