Lung-Ching Chen

Estimation of central systolic blood pressure using an oscillometric blood pressure monitor

Current noninvasive techniques for assessing central aortic pressure require the recording of an arterial pressure wave using a high-fidelity applanation tonometer. We therefore developed and validated a novel method to estimate the central aortic systolic pressure using an oscillometric blood pressure monitor alone. Invasive high-fidelity right brachial and central aortic pressure waves, and left-brachial pulse volume plethysmography from an oscillometric blood pressure monitor, were obtained at baseline and 3 min after administration of sublingual nitroglycerin in 100 patients during cardiac catheterization. In the initial 50 patients (Generation Group), Central systolic blood pressure was predicted by a multi-variate prediction model generated from the comprehensive analysis of the invasive brachial pressure wave, including brachial late-systolic shoulder pressure value and parameters related to wave reflection and arterial compliance. Another prediction model was similarly constructed from the noninvasively calibrated pulse volume plethysmography. Both models were validated in the subsequent 50 patients (Validation Group) with results: r=0.98 (P<0.001) and mean difference=0.5±4.5 (95% confidence interval −8.3 to 9.3) mm Hg for the invasive model, and r=0.93 (P<0.001) and mean difference=−0.1±7.6 (95% confidence interval −15.0 to 14.8) mm Hg for the noninvasive model. Thus, our results indicate that central aortic systolic blood pressure could be estimated by analysis of the noninvasive brachial pressure wave alone from an oscillometric blood pressure monitor.

Impaired forearm reactive hyperemia is related to late restenosis after coronary stenting

To investigate whether systemic endothelial function on forearm resistance vessels is related to angiographic restenosis after coronary stenting, 47 men who underwent elective coronary stenting were divided into 2 groups according to the presence (n = 20) or absence (n = 27) of in-stent restenosis 6 months after the procedure. Another 19 risk factor-matched men with normal coronary angiograms served as the control group. Forearm blood flow was assessed by venous occlusive plethysmography. Basal forearm blood flow was similar between restenosis, nonrestenosis, and control groups (2.63 +/- 0.19, 2.58 +/- 0.14, and 3.23 +/- 0.13 ml/100 ml forearm tissue per minute, respectively). In all 3 groups, forearm blood flow increased significantly during reactive hyperemia (5.75 +/- 0.7, 11. 32 +/- 1.23, and 14.52 +/- 1.36 ml/100 ml forearm tissue per minute, p <0.05, respectively) and remained unchanged after sublingual administration of nitroglycerin. The percentage change of forearm blood flow during reactive hyperemia was significantly lower in the restenosis group (117.3 +/- 18.3%) than in the nonrestenosis group (354.2 +/- 46.5%, p <0.01). This difference was still present after sublingual nitroglycerin (37.6 +/- 21.2% vs 226.4 +/- 40.5%, p <0. 01). In contrast, percentage change of hyperemic forearm blood flow was significantly lower in patients with angina (117.5 +/- 49.5%) than in those without angina (290.1 +/- 37.4%, p <0.05) at follow-up. In all patients, the angiographic loss index was correlated negatively to the percentage change of hyperemic forearm blood flow (r = -0.33, p <0.01) and positively to the percentage change of forearm vascular resistance during reactive hyperemia (r = 0.33, p <0.01). In patients with angiographic restenosis after coronary stenting, forearm reactive hyperemia was more impaired compared with those without angiographic restenosis. Systemic endothelial dysfunction might be either a marker or one of the confounding factors in the development of late restenosis after coronary stenting.

Coronary revascularization in a patient with immune thrombocytopenic purpura.

Immune thrombocytopenic purpura (ITP) is a bleeding disorder characterized by premature platelet destruction mediated by autoantibodies. We report a 71-year-old ITP patient with concomitant acute coronary syndrome. Cardiac catheterization was performed through the right radial artery and premedicated with immunoglobulin. Left anterior descending artery was stented, followed by clopidogrel treatment for 7 weeks without major bleeding complication. The patient has been observed for 2 years without clinical restenosis. We suggest that stent implantation is a safe treatment in this special condition. Treatment should be individualized, but it is still a challenge to balance bleeding and thrombosis complication.

Clinical and angiographic determinants of adverse cardiac events in patients with stent restenosis

Patients with angiographically proven stent restenoses do not necessarily develop adverse cardiac events. Which clinical, procedural, or angiographic parameters relate to the development of adverse cardiac events among these patients has not been determined. This study included 155 patients (167 stented lesions) with angiographically proven restenosis (≥ 50% diameter stenosis) within the stent or at its margins in routine follow‐up angiograms that was obtained at 6.5 ± 3.6 months after successful stenting. Thirty‐six patients (22%) had adverse cardiac events (including unstable angina necessitating target lesion revascularization, acute myocardial infarction, or cardiac death) during follow‐up and 119 patients (78%) were event‐free. These two groups of patients were compared to determine the parameters related to adverse cardiac events. Univariate determinants of adverse events included hypertension (P = 0.023), unstable angina at initial presentation (P = 0.002), target lesion in proximal left anterior descending artery (P = 0.041), TIMI grade 0–2 flow in follow‐up angiograms (p < 0.001), impaired left ventricular function at follow‐up (P = 0.002), follow‐up minimal lumen diameter ≤ 0.6 mm (P = 0.003), follow‐up diameter stenosis > 75% (P = 0.005), late loss > 2 mm (P = 0.01), and loss index > 1.127 (P < 0.001). Multivariate analysis demonstrated hypertension (odds ratio, OR, = 3.6; P = 0.019), unstable angina at initial presentation (OR = 2.6; P = 0.007), TIMI grade 0–2 flow at follow‐up (OR = 2.8; P = 0.05), impaired LV function at follow‐up (OR = 4.2; P = 0.004), and loss index > 1.127 (OR = 3.6; P = 0.017) as independent risk factors for adverse cardiac events. Classification and regression tree analysis identified loss index > 1.127 and impaired LV function as the two strongest determinant of adverse cardiac event. Therefore, hypertensive patients whose initial clinical presentation were unstable angina should be managed carefully to optimize the angiographic results and, most importantly, followed up more closely for development of impaired LV function after coronary stenting in order to prevent the occurrence of adverse cardiac event at follow‐up. Cathet Cardiovasc Intervent 2002;55:331–337.

Entrapment of a Swan-Ganz catheter

Failure to withdraw a catheter is related primarily to catheter entrapment or knotting. Placement of a Swan-Ganz catheter is associated with various complications, one of which is entrapment. Entrapment of a Swan-Ganz catheter in the heart, vena cava, or pulmonary artery is a very rare and serious complication that may lead to life-threatening complications if not treated appropriately. Most reported cases of catheter entrapment have been associated with surgical sutures, artificial valves, or abnormal cardiac anatomy. Here we report a rare case of Swan-Ganz catheter entrapment resulting from inserting an excessive length of Swan-Ganz catheter into the heart. The catheter was removed smoothly under fluoroscopic guidance.