variety of factors are involved in the development of unstable angina pectoris (UAP), including coronary plaque rupture and thrombus formation, 1-3 coronary spasm, 4 and abnormalities in the coagulationfibrinolysis system, 2 and of these, coronary plaque rupture and thrombus formation are thought to be a direct cause. Studies involving autopsy specimens, 5,6 coronary arteriography, 7 intracoronary endoscopy, 8-10 intravascular ultrasound imaging 11 and directional coronary atherectomy (DCA) [12][13][14][15] have demonstrated the presence of thrombus in many patients with UAP. Although thrombus is known to be involved in the development of acute coronary syndromes, the mechanism for the acute deterioration of angina pectoris, resulting from intimal proliferation after interventional therapy such as percutaneous transluminal coronary angioplasty (PTCA) or DCA, has not been adequately investigated. It is unknown whether thrombus plays a role in producing angina in this setting, so the present study determined the incidence of such thrombi by examining tissue specimens collected at the time of DCA. Japanese Circulation Journal Vol.65, June 2001 MethodsThe study group consisted of 14 patients (16 arterial branches) with angina pectoris in whom PTCA or DCA was performed and who developed UAP after restenosis at the same site, and who then underwent DCA for the restenosed lesion (R-UAP group) ( Table 1). With respect to drug therapy after PTCA or DCA, all patients received nitrates and/or diltiazem in addition to ticlopidine (200 mg/day) and aspirin (81 mg/day) as anti-platelet agents. After the development of UAP, patients were admitted and given heparin (16,000-20,000 units/day) for 1-2 days by continuous intravenous infusion, with an additional 10,000 units intravenously at the time of DCA. The control groups consisted of 94 patients with no prior history of PTCA or DCA, including a group with UAP (P-UAP group; n=29, 29 branches), a group with acute myocardial infarction (AMI group; n=34, 34 branches), and a group with stable angina pectoris (SAP group; n=31, 33 branches), who underwent DCA. Heparin was given to the P-UAP group in the same way as in the R-UAP group.The mean age was 66.1±7.4 years in the R-UAP group, 60.0±7.2 years in the P-UAP group, 58.7±10.6 years in the AMI group, and 61.2±9.2 years in the SAP group. The diagnosis of UAP was based on the definition proposed by the American Heart Association. 16 The degree of angiographic stenosis before and after DCA was measured using the direct caliber method by 2 experienced cardiologists who were blinded to the patients' clinical diagnoses.After DCA, the number of fragments and the tissue weight of the resected material were determined. After being fixed in 10% buffered formalin, the specimens were The pathogenesis of unstable angina pectoris (UAP) following percutaneous transluminal coronary angioplasty (PTCA) or directional coronary atherectomy (DCA) has not been adequately investigated, so the present study aimed to determine whether thrombi are present in...

The activation-recovery interval (ARI), measured directly from the myocardium, has shown a good correlation with the action potential duration (APD) in experiments. APD has been reported to be inversely related to the activation time (AT). However, no studies have examined the correlation between the body-surface ARI and AT in normal subjects. Fifty normal subjects (25 men and 25 women) were studied to elucidate the relationship between the body-surface ARI and AT. The body-surface AT was defined as the duration between the QRS onset and the minimum dV/dt of the QRS wave, and ARI as the interval between the minimum dV/dt of the QRS wave and the maximum dV/dt of the T wave in each lead of an 87 unipolar lead system. We also measured the recovery time (RT) defined as the duration between the QRS onset and the maximum dV/dt of the T wave. ARI was inversely correlated with AT (r = -0.73). RT was also inversely correlated with AT (r = -0.61), however, RT had a less heterogeneous distribution than ARI (148 ms vs 159 ms). There were no differences between male and female subjects in the relation between ARI and RT or in the body-surface distribution of ARI and RT. These findings suggest that the body-surface ARI may reflect recovery properties over the cardiac surface and that APD may distribute inhomogeneously over the human cardiac surface with a longer RT over an area with a shorter AT. ARI calculated from body-surface ECG may be a useful noninvasive and repeatedly measurable estimate of APD.

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