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Objectives The purpose of this study was to evaluate long-term clinical impact of routine follow-up coronary angiography (FUCAG) after percutaneous coronary intervention (PCI) in daily clinical practice in Japan. Background The long-term clinical impact of routine FUCAG after PCI in real-world clinical practice has not been evaluated adequately. Methods In this prospective, multicenter, open-label, randomized trial, patients who underwent successful PCI were randomly assigned to routine angiographic follow-up (AF) group, in which patients were to receive FUCAG at 8 to 12 months after PCI, or clinical follow-up alone (CF) group. The primary endpoint was defined as a composite of death, myocardial infarction, stroke, emergency hospitalization for acute coronary syndrome, or hospitalization for heart failure over a minimum of 1.5 years follow-up. Results Between May 2010 and July 2014, 700 patients were enrolled in the trial among 22 participating centers and were randomly assigned to the AF group (n = 349) or the CF group (n = 351). During a median of 4.6 years of follow-up (interquartile range [IQR]: 3.1 to 5.2 years), the cumulative 5-year incidence of the primary endpoint was 22.4% in the AF group and 24.7% in the CF group (hazard ratio: 0.94; 95% confidence interval: 0.67 to 1.31; p = 0.70). Any coronary revascularization within the first year was more frequently performed in AF group than in CF group (12.8% vs. 3.8%; log-rank p Conclusions No clinical benefits were observed for routine FUCAG after PCI and early coronary revascularization rates were increased within routine FUCAG strategy in the current trial. (Randomized Evaluation of Routine Follow-up Coronary Angiography After Percutaneous Coronary Intervention Trial [ReACT]; NCT01123291)

The prevalence, intensity, safety, and efficacy of oral anticoagulation (OAC) in addition to dual antiplatelet therapy (DAPT) in “real-world” patients with atrial fibrillation (AF) undergoing percutaneous coronary intervention (PCI) have not yet been fully evaluated. In the Coronary REvascularization Demonstrating Outcome Study in Kyoto registry cohort-2, a total of 1,057 patients with AF (8.3%) were identified among 12,716 patients undergoing first PCI. Cumulative 5-year incidence of stroke was higher in patients with AF than in no-AF patients (12.8% vs 5.8%, p

Therapeutic strategies preventing late target lesion revascularization (TLR) after drug-eluting stent implantation have not been yet adequately investigated. In 13,087 consecutive patients undergoing first percutaneous coronary intervention in the CREDO-Kyoto Registry Cohort-2, we identified 10,221 patients who were discharged alive after implantation of sirolimus-eluting stents (SESs) only (SES stratum 5,029) or bare-metal stents (BMSs) only (BMS stratum 5,192). Impact of statin therapy at time of discharge from the index hospitalization on early (within the first year) and late (1 year to 4 years) TLR, was assessed in the SES stratum (statin group 2,735; nonstatin group 2,294) and in the BMS stratum (statin group 2,576; nonstatin group 2,616). Despite a significantly lower incidence of early TLR (7.8% vs 22.2%, p

Background— There still remain safety concerns on surgical procedures after coronary drug-eluting stents (DES) implantation, and optimal management of perioperative antiplatelet therapy (APT) has not been yet established. Methods and Results— During 3-year follow-up of 12 207 patients (DES=6802 patients and bare-metal stent [BMS] only=5405 patients) who underwent coronary stent implantation in the CREDO-Kyoto registry cohort-2, surgical procedures were performed in 2398 patients (DES=1295 patients and BMS=1103 patients). Surgical procedures (early surgery in particular) were more frequently performed in the BMS group than in the DES group (4.4% versus 1.9% at 42-day and 23% versus 21% at 3-year, log-rank P =0.0007). Cumulative incidences of death/myocardial infarction (MI)/stent thrombosis (ST) and bleeding at 30 days after surgery were low, without differences between BMS and DES (3.5% versus 2.9%, P =0.4 and 3.2% versus 2.1%, P =0.2, respectively). The adjusted risks of DES use relative to BMS use for death/MI/ST and bleeding were not significant (hazard ratio: 1.63, 95% confidence interval: 0.93 to 2.87, P =0.09 and hazard ratio: 0.6, 95% confidence interval: 0.34 to 1.06, P =0.08, respectively). The risks of perioperative single- and no-APT relative to dual-APT for both death/MI/ST and bleeding were not significant; single-APT as compared with dual-APT tended to be associated with lower risk for death/MI/ST (hazard ratio: 0.4, 95% confidence interval: 0.13 to 1.01, P =0.053). Conclusions— Surgical procedures were commonly performed after coronary stent implantation, and the risk of ischemic and bleeding complications in surgical procedures was low. In patients selected to receive DES or BMS, there were no differences in outcomes. Perioperative administration of dual-APT was not associated with lower risk for ischemic events.

Long-term safety and efficacy of drug-eluting stents remains controversial. The CREDO-Kyoto registry cohort-2 is a physician-initiated non-company sponsored multi-center registry enrolling consecutive patients undergoing first coronary revascularization in 26 centers in Japan. We compared 3-year outcome between patients treated with sirolimus-eluting stent (SES) only (5092 patients) and bare-metal stent (BMS) only (5405 patients). SES-use as compared with BMS-use was associated with significantly lower adjusted risk for all-cause death [hazard ratio (HR) [95% confidence interval (CI)] 0.72 (0.59–0.87), P = 0.0007], which was mainly driven by the reduction in non-cardiac death [HR (95% CI) 0.64 (0.48–0.85), P = 0.002]. The risk of cardiac death [HR (95% CI) 0.82 (0.63–1.07), P = 0.15], myocardial infarction [HR (95% CI) 0.73 (0.51–1.03), P = 0.07] and definite stent thrombosis [HR (95% CI) 0.62 (0.35–1.09), P = 0.1] was not different between the two groups. Despite longer duration of thienopyridine administration, SES-use was associated with significantly lower risk for bleeding [HR (95% CI) 0.75 (0.6–0.95), P = 0.02] and similar risk for stroke [HR (95% CI) 1.0 (0.75–1.34), P = 1.0]. The risk for target-lesion revascularization (TLR) was markedly lower in the SES group [HR (95% CI) 0.42 (0.36–0.48), P < 0.0001]. The direction and magnitude of the effect of SES relative to BMS in patients presenting acute myocardial infarction (AMI) were similar to those in patients presenting otherwise. In conclusion, SES-use as compared with BMS-use was associated with marked reduction of TLR without any increases in death, myocardial infarction, stent thrombosis, stroke and bleeding in real world clinical practice regardless of clinical presentation including AMI.

Previous studies have shown inconsistent results regarding the effects of concomitant use of clopidogrel and proton pump inhibitors (PPI) on cardiovascular outcomes. We sought to evaluate the clinical impact of PPI-use in patients treated with thienopyridines after percutaneous coronary intervention (PCI) in a large Japanese observational database. Among 12446 patients discharged alive on thienopyridines (ticlopidine 90.4% and clopidogrel 9.6%), 3223 patients were treated with PPIs and 9223 patients without PPI at the time of hospital discharge. The PPI group included more patients with co-morbidities than the non-PPI group. The adjusted hazard ratio (HR) of PPI-use for a composite of cardiovascular death, myocardial infarction, and stroke was 1.26 (95% confidence interval (CI) 1.09-1.47, p = 0.002). The adjusted HR of PPI-use for bleeding was 1.26 (95% CI 1.05-1.52, p = 0.013). Cardiovascular and bleeding outcomes were not different among the three groups receiving three different types of PPI. The negative effect of PPI on cardiovascular outcome was consistently seen in both drug-eluting stent (DES) [HR 1.31 (95% CI 1.07-1.6, p = 0.0097)] and non-DES strata [HR 1.25 (95% CI: 0.99-1.57, p = 0.057)] (Interaction p = 0.79) despite the fact that the duration of thienopyridine administration was significantly longer in patients receiving DES. In conclusion, cardiovascular outcomes after PCI were significantly worse in patients with PPI than in patients without PPI in the Japanese real clinical practice. However, the observed poorer cardiovascular outcome in patients receiving PPI was most likely to be related to residual confounding and seemed not causally related to attenuation of antiplatelet effect of thienopyridine through interaction with PPI.

Objectives This study evaluated safety and efficacy of upfront thrombus aspiration during primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI). Background Distal embolization during primary PCI results in reduced myocardial perfusion and poor clinical outcomes. Methods The VAMPIRE (VAcuuM asPIration thrombus REmoval) study was a prospective, randomized, controlled multicenter trial conducted in 23 institutions. Patients (N = 355) presenting within 24 h of STEMI symptoms onset were randomized to primary PCI with (n = 180) or without (n = 175) upfront thrombus aspiration using Nipro's TransVascular Aspiration Catheter (Osaka, Japan). Results The TransVascular Aspiration Catheter reached the lesion in 100% of cases. It successfully crossed the target obstruction in 86% without any delay in procedure time or time to reperfusion; whereas macroscopic thrombi were removed in 75% of the cases. Procedure success was similar between groups (98.9% vs. 98.3%). There was a trend toward lower incidence of slow or no reflow (primary end point—defined as a Thrombolysis In Myocardial Infarction flow grade l3) in patients treated with aspiration versus conventional primary PCI (12.4% vs. 19.4%, p = 0.07). Rate of myocardial blush grade 3 was higher in the aspiration group (46.0% vs. 20.5%, p l 0.001). Aspiration was most effective in patients presenting after 6 h of symptoms onset (slow flow rate: 8.1% vs. 37.6%, p = 0.01). Conclusions This study suggested the safety of primary PCI with upfront thrombectomy using a novel device in patients with STEMI. The study showed a trend toward improved myocardial perfusion and lower clinical events in patients treated with aspiration. Patients presenting late after STEMI appear to benefit the most from thrombectomy.

Background Adjunctive thrombus aspiration ( TA ) during primary percutaneous coronary intervention ( PCI ) was reported to promote better coronary and myocardial reperfusion. However, long‐term mortality benefit of TA remains controversial. The objective of this study is to investigate the clinical impact of TA on long‐term clinical outcomes in patients with ST ‐segment elevation myocardial infarction (STEMI) undergoing primary PCI . Methods and Results The CREDO ‐Kyoto AMI Registry is a large‐scale cohort study of acute myocardial infarction patients undergoing coronary revascularization in 2005–2007 at 26 hospitals in Japan. Among 5429 patients enrolled in the registry, the current study population consisted of 3536 patients who arrived at the hospital within 12 hours after the symptom onset and underwent primary PCI . Clinical outcomes were compared between the 2 patient groups with or without TA . During primary PCI procedures, 2239 out of 3536 (63%) patients underwent TA ( TA group). The cumulative 5‐year incidence of all‐cause death was significantly lower in the TA group than in the non‐ TA group (18.5% versus 23.9%, log‐rank P TA group was not significantly lower than that in the non‐ TA group (hazard ratio: 0.90, 95% CI : 0.76 to 1.06, P =0.21). The adjusted risks for cardiac death, myocardial infarction, stroke, and target‐lesion revascularization were also not significantly different between the 2 groups. Conclusions Adjunctive TA during primary PCI was not associated with better 5‐year mortality in STEMI patients.

Although a robust relationship between aberrant serum polyunsaturated fatty acids (PUFAs) profile and coronary artery disease (CAD) has been reported, the details concerning the association between aberrant PUFAs profile and clinical feature of CAD are not fully discovered. Therefore, we investigated the relationship between serum PUFAs and clinical profiles in CAD patients. We classified 595 consecutive CAD patients, who underwent coronary angiography into 3 groups according to the clinical profiles of CAD (group A: early phase ACS, n = 96; group B: stable CAD with previous history of ACS, n = 259; group C: stable CAD without previous history of ACS, n = 240) and measured serum n-3 [eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA)] and n-6 [arachidonic acid (AA)] PUFAs. Serum EPA, DHA, and EPA/AA ratio were significantly low in the order of group A

Background— Late adverse events such as very late stent thrombosis (VLST) or late target-lesion revascularization (TLR) after first-generation sirolimus-eluting stents (SES) implantation have not been yet fully characterized at long term in comparison with those after bare-metal stent (BMS) implantation. Methods and Results— Among 13 058 consecutive patients undergoing first percutaneous coronary intervention in the Coronary REvascularization Demonstrating Outcome study-Kyoto registry Cohort-2, 5078 patients were treated with SES only, and 5392 patients were treated with BMS only. During 7-year follow-up, VLST and late TLR beyond 1 year after SES implantation occurred constantly and without attenuation at 0.24% per year and at 2.0% per year, respectively. Cumulative 7-year incidence of VLST was significantly higher in the SES group than that in the BMS group (1.43% versus 0.68%, P P =0.91). Cumulative incidences of late TLR (both overall and clinically driven) were also significantly higher in the SES group than in the BMS group (12.0% versus 4.1%, P P Conclusions— Late catch-up phenomenon regarding stent thrombosis and TLR was significantly more pronounced with SES than that with BMS. This limitation should remain the target for improvements of DES technology.

Abstract Tissue factor is a membrane-bound glycoprotein that functions in the extrinsic pathway of blood coagulation by acting as a cofactor for factor VII, and the resulting complex leads to thrombin production in vivo. The purpose of the present study is to determine whether macrophages express tissue factor in human coronary atherosclerotic plaques. We examined directional coronary atherectomy specimens from 24 patients with unstable angina and 23 with stable exertional angina. In these specimens, macrophages were detected in 22 (92%) of 24 patients with unstable angina versus 12 (52%) of 23 with stable exertional angina ( P =.003). The percentage of macrophage infiltration area was significantly larger in patients with unstable angina than in those with stable exertional angina (17±3% versus 6±2%, P =.008). The immunohistochemical double staining revealed the expression of tissue factor on macrophages in 18 (75%) of 24 patients with unstable angina versus 3 (13%) of 23 with stable exertional angina ( P P =.02). Fibrin deposition was mainly observed around macrophages expressing tissue factor in the patients with unstable angina. We have shown that tissue factor expression on macrophages was more frequent in coronary atherosclerotic plaques in patients with unstable angina. Tissue factor expressed on macrophages may play an important role in the thrombogenicity in coronary atherosclerotic plaques of these patients.

Methods From May 1 to September 6 in 2012, 31 consecutive patients received whole heart coronary MRA without contrast medium in 3T MRI scanner (Ingenia 3.0T, Philips Healthcare). 26 patients (84%) had sufficient quality to analyze. In these, 21 patients (16 men; mean age 69 years) received coronary angiography within 1 month of MRA. In MRA, coronary arteries were segmented to proximal, mid, distal RCA (segment 1, 2, 3), LMT (segment 5), proximal, mid, distal LAD (segment 6, 7, 8), and proximal, distal LCX (segment 11, 13). In coronary angiography, a stenosis of over 50% was defined to be significant. The segments after stent implantation were excluded.

Despite advances in the study of exercise for acute myocardial infarction (AMI) patients, few studies on exercise for post-AMI heart rupture patients have been reported. We assessed three cases of heart rupture (of the left ventricular free wall in two cases and of the ventricular septum in one case) in post-AMI patients who underwent three-graded exercise. Two of the three patients were operated on, whereas one patient was managed conservatively for heart rupture. Two of the three cases had also suffered cerebral infarction post-AMI. The exercise program was composed of three grades, slow level walking (grade 1), mild reconditioning and activities of daily living (ADL) exercises (grade 2), and optional endurance training using machines below 75% of predicted maximal heart rate (grade 3). Electrocardiograms and blood pressure were monitored during all exercises. All patients had muscle weakness, poor endurance capacity, as well as low cardiac function (28-47% of left ventricular ejection fraction). Two patients underwent grades 1 and 2 exercise programs, and the other performed grades 1, 2, and 3 exercise programs over a 3- to 10-wk period. We observed improvement in the double product, work capacity, and ADL without congestive heart failure, ischemic attack, or serious arrhythmias. However, the youngest patient, who underwent the grade 3 exercise program, died from a cardiac event 10 mo after onset of AMI. We conclude that post-AMI heart rupture patients should undergo delayed, gradual, low-level graded exercise (4-6 metabolic equivalents), with monitoring of blood pressure and electrocardiograms to improve work capacity, ADL, and the quality of life. However, daily activity and exercise intensity should be promptly supervised for those with severely deteriorated cardiac functions to prevent sudden cardiac event.

症例は27歳,女性.検診にて胸部X線異常陰影を指摘され受診.呼吸困難,チアノーゼを認め,心エコーでは右室壁肥厚,大動脈騎乗,心室中隔欠損を認めた.心血管造影施行,右室造影にて肺動脈閉鎖,大動脈騎乗,心室中隔欠損を認め,大動脈造影にて両肺へのmajor aortopulmonary collateral artery (MAPCA)を認め, MAPCAを伴うFallot四徴症と診断した. MAPCAを伴うFallot四徴症の未手術での成年症例は稀であるので報告した.

Background— Optimal duration of dual antiplatelet therapy (DAPT) after drug-eluting stent (DES) implantation has not been yet fully elucidated. Methods and Results— We assessed the influence of prolonged thienopyridine therapy on clinical outcomes with landmark analysis at 4 and 13 months after DES implantation. Among 6802 patients with at least 1 DES implantation in the CREDO-Kyoto Registry Cohort-2, 6309 patients (on thienopyridine, 5438 patients; off thienopyridine, 871 patients) and 5901 patients (on thienopyridine, 4098 patients; off thienopyridine, 1803 patients) were eligible for the 4- and 13-month landmark analyses, respectively. The majority of patients had stable coronary artery disease (73%) and received sirolimus-eluting stents (93%), and approximately 90% of thienopyridine was ticlopidine. Patients taking thienopyridine had more complex comorbidities and more complex lesion and procedural characteristics as compared with patients not taking thienopyridine. After adjusting for confounders, thienopyridine use was not associated with decreased risk for death/myocardial infarction/stroke (hazard ratio [HR], 1.13; 95% confidence interval [CI], 0.89–1.43, P =0.32 in the 4-month landmark analysis; HR, 1.14; 95% CI, 0.90–1.45, P =0.29 in the 13-month landmark analysis, respectively), whereas the risk for GUSTO moderate/severe bleeding tended to be higher in patients taking thienopyridine (HR, 1.51; 95% CI, 1.00–2.23, P =0.049 in the 4-month landmark analysis; HR, 1.44; 95% CI, 0.99–2.09, P =0.057 in the 13-month landmark analysis, respectively). Conclusions— Prolonged thienopyridine therapy beyond 4 and 13 months appeared not to be associated with reduction in ischemic events but to be associated with a trend toward increased bleeding. Optimal duration of DAPT after DES implantation might be shorter than the currently recommended 1-year interval.

This study evaluated safety and efficacy of upfront thrombus aspiration during primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI).Distal embolization during primary PCI results in reduced myocardial perfusion and poor clinical outcomes.The VAMPIRE (VAcuuM asPIration thrombus REmoval) study was a prospective, randomized, controlled multicenter trial conducted in 23 institutions. Patients (N = 355) presenting within 24 h of STEMI symptoms onset were randomized to primary PCI with (n = 180) or without (n = 175) upfront thrombus aspiration using Nipro's TransVascular Aspiration Catheter (Osaka, Japan).The TransVascular Aspiration Catheter reached the lesion in 100% of cases. It successfully crossed the target obstruction in 86% without any delay in procedure time or time to reperfusion; whereas macroscopic thrombi were removed in 75% of the cases. Procedure success was similar between groups (98.9% vs. 98.3%). There was a trend toward lower incidence of slow or no reflow (primary end point-defined as a Thrombolysis In Myocardial Infarction flow grade3) in patients treated with aspiration versus conventional primary PCI (12.4% vs. 19.4%, p = 0.07). Rate of myocardial blush grade 3 was higher in the aspiration group (46.0% vs. 20.5%, p0.001). Aspiration was most effective in patients presenting after 6 h of symptoms onset (slow flow rate: 8.1% vs. 37.6%, p = 0.01).This study suggested the safety of primary PCI with upfront thrombectomy using a novel device in patients with STEMI. The study showed a trend toward improved myocardial perfusion and lower clinical events in patients treated with aspiration. Patients presenting late after STEMI appear to benefit the most from thrombectomy.

Background: The difference in the effect of cardiac resynchronization therapy (CRT) in patients with non-ischemic cardiomiopathy (NICM) and RV pacing-induced cardiomyopathy (PACING) hasn’t been fully estimated. Methods and Results: We investigated the effect of CRT between 6 to 12 months after implantation of ischemic cardiomyopathy (ICM), NICM and Pacing group. LV end-systolic diameter (ESD) on echocardiography and serum BNP level before and after CRT implantation were evaluated. Fourty patients (ICM: 9 patients, NICM: 22 patients, PACING: 9 Patients) were implanted CRT-P or CRT-D between January 2006 to September 2010. CRT-P was implanted in 14 patients and CRT-D was in 26 patients. At baseline, ESD and BNP level showed no significant differences among 3 groups. On follow-up periods, ESD and BNP level didn’t change in ICM group (ESD: from 62.3±6.7 to 58.3±7.5 mm, BNP: from 530.9±388.0 to 496.4±280.0 ng/ml, both p=NS). In NICM group, BNP level was significantly decreased but ESD was not (ESD: from 54.3±9.8 to 53.5±10.5 mm, p=NS, BNP: from 583.2±406.6 to 339.7±238.7 ng/ml, p

A 76-year-old man, with previous history of dilated cardiomyopathy and ventricular tachycardia treated with amiodarone was admitted to our hospital because of intestitial pneumonia. After discontinuation of amiodarone, VT was occurred frequently. VT’s cycle length (CL) was 465 ms and QRS morphology was LBBB+LAD. Even after nifekalant administration, VT storm was uncontrollable. Frequent cardioversion and sedation were needed. After d-sotalol administration, cathether ablation was performed with electro-anatomical mapping (CARTO). The substrate map of RV revealed low voltage zone in anterior wall and RVOT. VT was inducted easily with programmed stimulations at RVA and RVOT, so this VT’s mechanism thought to be reentry. But the centrifugal electric potential from RVOT anterior wall was confirmed in activation map. The CL on activation map was covered only 200 ms, the reentry circuits may be located in the epicardium. The earliest ventricular activation site was 100 ms prior to the QRS onset on endocardium at RVOT. Radiofrequency energy was delivered around this site and linear ablation was performed in low voltage zone between tricuspid annulus and anterior wall. Finally, clinical VT couldn’t be inducted by programmed stimulation and didn’t occurred during follow up period. In this case, VT origin may present at RV epicardium which was controlled with ablation and d-sotalol.

A 74-year-old man with previous myocardial infarction and CABG was admitted our hospital because of sustained VT. VT’s cycle length (CL) was 460 ms and QRS morphology was RBBB+LAD (VT1). As he had intestinal pneumonia, amiodarone was contraindicated. Thus we started nifekalant and d-sotalol. VT was controlled by nifekalant, but relapsed and became uncontrollable after discontinuation of nifekalant, even with increased dosage of d-sotalol. Temporary pacing from RVA wasn’t effective, and QT interval became be more prolonged after increased dosage of nifekalant and d-sotalol. Thus catheter ablation was performed. Clinical VT couldn’t induced by programmed stimulations at RVA and RVOT. Perfect pacemap site was existed at inferoseptal wall. At this site, purkinje potential preceded ventricular potential. Radiofrequency (RF) energy was delivered around this site. Next evening, altenated VT was appeared. QRS morphologies were LBBB+LAD (VT2, CL: 440 ms) and RBBB+superior axis (VT3, CL: 520 ms). After we administration of nifekalant, VT was supressed. After ICD implantation, we stopped d-sotalol and started bepridil. VT duration became shorter, but its frequency showed no change. We performed catheter ablation again because of repetitive VT. VT couldn’t induced on this session, either. RF energy was delivered at perfect (VT2, midseptal) and good (VT3, inferoseptal, slightly anterior of VT1) pacemap site. Linear lesion was made in low voltage zone between two pacemap sites and between septal and anterior wall. After ablation, VT dissappeared with low dose bepridil. Conclusion: Alterated VT modified by focal ablation was effective linear ablation at low voltage zone and pottasium channel blocker.

To quantify the effects of early reperfusion on the size of infarcts, an enzyme indicator was developed: myocardial creatine kinase (CK) release rate (kr), based on a compartmental kinetics model. In 59 patients with acute myocardial infarction (MI) who received intracoronary thrombolysis therapy in the acute phase, the kr showed a good correlation with the flow condition of infarct-related coronary artery and the time required to reach peak enzyme activity. Apparent serum CK disappearance rate (kd') was estimated by using the method of Norris. The kd' was significantly underestimated in patients without reperfusion, suggesting the presence of prolonged enzyme release from the infarcted area. In 22 of 59 patients, who had a first acute anterior MI (left anterior descending arterial lesion), the correction of cumulative enzyme release by myocardial enzyme release (kr) resulted in a closer correlation with chronic phase left ventricular function. Thus, kinetic analyses of serum enzyme release provide a useful means to estimate the infarct size during intracoronary thrombolysis therapy.

Coronary arteriographic findings during an attack of angina pectoris associated with S-T segment elevation and angina associated with S-T depression were compared in 54 patients. Thirty-eight attacks with S-T segment elevation included 2 that were spontaneous, 6 induced by methacholine, 4 by epinephrine with or without propranolol, 9 by arm exercise, 5 by hyperventilation with or without Tris-buffer infusion and 12 by ergonovine maleate. Twenty-nine of the 38 attacks were associated with total occlusion, 8 with subtotal occlusion and 1 with diffuse narrowing of a major coronary artery caused by spasm. Twenty-six attacks with S-T segment depression included 3 induced by methacholine, 13 by arm exercise, 3 by hyperventilation with or without Tris-buffer infusion and 7 by ergonovine maleate. Eight of the 26 attacks were associated with subtotal occlusion and 9 with diffuse narrowing of a major coronary artery caused by spasm; 3 attacks were associated with total occlusion of a major coronary artery well supplied with collateral vessels and 2 with total occlusion of a small coronary branch caused by spasm. Four attacks were associated not with spasm but with fixed subtotal occlusion of a major coronary artery (3 attacks) or total occlusion of a major coronary artery receiving collateral vessels (1 attack). Only 2 of the 31 patients with S-T segment elevation had collateral vessels compared with 8 of the 16 patients with S-T segment depression (p less than 0.001). It is concluded that angina pectoris associated with S-T segment elevation usually indicates more severe myocardial ischemia than angina associated with S-T segment depression.

Vigorous hyperventilation was induced for five minutes immediately after a five-minute infusion of 100 ml of Tris-buffer (pH 10) in nine patients with Prinzmetal's variant angina. In eight of the patients, chest pain with ischemic changes in the electrocardiogram occurred during this procedure or within five minutes after it ended. Coronary arterial spasm appeared after the procedure and disappeared after the administration of nitroglycerin in all four patients in whom coronary cinearteriography was performed. This was evident both before and after the procedure and after sublingual administration of nitroglycerin (0.6 mg). The oral administration of 90 mg of diltiazem, a calcium antagonistic drug, two hours before, completely suppressed the attack induced by the procedure in all of the five patients who received this drug. We conclude that hyperventilation plus Tris-buffer infusion induces coronary arterial spasm and anginal attack in patients with Prinzmetal's variant angina and that diltiazem suppresses these reactions.

To twenty six patients with angina at rest (including 13 patients with Prinzmetal's variant angina), propranolol 40--50 mg, dilitiazem 60--90 mg, dipyridamole 50 mg, atropine sulfate 0.6 mg and phenoxybenzamine 10--20 mg were given at 9:00 p.m. and 2:00 a.m. (except phenoxybenzamine which was given only at 9:00 p.m.) to examine the effect of these drugs on the attack. Propranolol was not only ineffective in suppressing the attack but rather tended to aggravate it in all the cases of Prinzmetal's variant angina. It was effective to some degree in 5 of 13 cases of angina at rest other than Prinzmetal's variant angina. Diltiazem suppressed the attack completely and dramatically in all the cases of angina at rest (including Prinzmetal's variant angina). Dipyridamole was ineffective in all the cases except one in suppressing the attack. Atropine sulfate and phenoxybenzamine suppressed the attack in 13 of 21 cases and in 6 of 12 cases respectively. Coronary arteriography was done before and after the intravenous administration of 10 mg of diltiazem in 8 patients and it was demonstrated that diltiazem dilates large coronary arteries in all these patients. It is concluded that diltiazem, a calcium antagonistic drug, is specifically effective in suppressing the attack of angina at rest by dilating large coronary arteries and that the autonomic nervous system plays a role in the genesis of the attack probably by constricting large coronary arteries by way of alpha adrenergic receptors.

We examined the pathogenesis of angina pectoris in 101 patients with one-vessel disease except those with 99% to 100% occlusion. The attacks could not be induced or could not be reproducibly induced by maximal treadmill exercise at the same hour of different days within a week period in 54 (53.5%) of the patients. In the 47 patients whose attacks were reproducibly induced by the exercise, propranolol, 80 mg orally, did not suppress the attacks in 41 (87.2%) of the patients. Diltiazem, 90 mg, and nifedipine, 20 mg given orally, suppressed the attacks completely in 39 (83.0%) of the 47 patients and in 36 (81.8%) of the 44 patients, respectively. Coronary arteriography showed that dynamic obstruction of the artery supplying the area of myocardium represented by ST segment deviation appeared during the attacks and disappeared with subsidence of the attacks in all 55 patients in whom coronary arteriography was done during the attack. We conclude that angina pectoris is usually caused not by increased myocardial oxygen demand but by dynamic coronary obstruction or by a combination of both in most patients with one-vessel disease.

A 45-year-old woman with almost normal coronary arteries suffered from acute inferior myocardial infarction after taking 2 tablets (2.0 mg) of ergotamine tartrate for headache. She had had attacks of variant angina and spasm of the right coronary artery had been demonstrated during the attack. After the recovery from myocardial infarction the intravenous injection of ergonovine maleate 0.05 mg induced spasm of the right coronary artery again. We conclude that acute myocardial infarction in this patient was probably caused by coronary arterial spasm induced by ergotamine tartrate.

The effect of diltiazem on left ventricular isovolumic relaxation time was examined in 11 patients with hypertrophic obstructive and non-obstructive cardiomyopathy in a combined study using phonocardiograms and echocardiograms. Five to 10 min after intravenous injection of diltiazem (0.2 mg/kg, body weight), a prolonged isovolumic left ventricular relaxation time, which was measured from aortic component of the second heart sound to the mitral opening on the echocardiogram, decreased from 63.1 +/- 26.0 to 46.9 +/- 28.0 msec (p less than 0.01). This study suggests that diltiazem, one of the calcium blocking agents, may ameliorate the impaired left ventricular diastolic function in patients with hypertrophic cardiomyopathy.

We performed coronary arteriography and gave intracoronary injection of nitrates within 8 hours after the onset of symptoms of acute myocardial infarction in eighteen patients. Improved distal filling or patency of the total occluded coronary artery after intracoronary injection of nitrates occurred in 4 of 18 patients. In one of four patients the first intracoronary nitrates injection failed to release the initial total occlusion, but after intracoronary Urokinase administration, the second nitrates injection succeeded to dilate the com pletely occluded coronary artery. Coronary arteriography was again per formed in sixteen patients in the chronic stage (4-15 weeks after the onset of acute myocardial infarction) and ergonovine malaete was injected intraven ously in seven patients. Focal spasm was induced by ergonovine injection in three patients in one of whom intracoronary nitrates failed to release the complete obstruction in the acute stage. We conclude that coronary spasm as well as intracoronary thrombosis plays an important role in the production of acute myocardial infarction.

A 37-year-old female who delivered her second child via a cesarean section 4 months previously presented to our hospital with gradual worsening of dyspnea on effort. Chest radiographic appearance showed cardiomegaly (cardiothoracic ratio 61%) and slight bilateral pulmonary congestion. Echocardiogram revealed diffuse hypokinesis of both left and right ventricles (left ventricular ejection fraction 29%) and large biventricular thrombus [left ventricular apex (28mm×21mm, 22mm×14mm) and right ventricular apex (16mm×11mm)]. She was diagnosed as having peripartum cardiomyopathy (PPCM) and anticoagulation therapy was started. Surgical thrombectomy was not selected because of risk of complications. Massive cerebral infarction occurred 10 days after diagnosis. She was discharged with aphasia and right incomplete hemiplegia 65 days after admission. Biventricular thrombus is a rare complication of PPCM. If high risk of massive embolism is considered, surgical thrombectomy may be warranted even in cases with low cardiac function. Learning objective: Biventricular thrombus is a rare complication of peripartum cardiomyopathy (PPCM). We report a case of biventricular thrombus secondary to PPCM. The decision to perform prophylactic surgical approach to ventricular thrombus is difficult in cases with low cardiac function.>

Thirteen patients with Prinzmetal's variant angina performed treadmill exercise tests in the early morning and in the afternoon of the same day. The attacks with ST elevation were induced repeatedly in all 13 patients in the early morning, but in only two patients in the afternoon. Propranolol did not suppress the exercise-induced attacks in all 13 patients. Diltiazem suppressed the attacks in all 13 patients and phentolamine in eight of the nine patients. Coronary arteriograms demonstrated that spasm occluding completely or almost completely the large coronary artery supplying the area of myocardium showing ST elevation appeared during the attacks and disappeared along with the attacks after nitroglycerin administration in all four patients in whom the attacks were induced by arm exercise in the catheterization laboratory. We conclude that there is circadian variation of exercise capacity in patients with Prinzmetal's variant angina caused by coronary arterial spasm induced by exercise in the early morning but not in the afternoon.

Two hundred forty-five patients with variant angina were followed for an average of 80.5 months (range, 36-184 months). Survival rate at 1, 3, 5, and 10 years was 98%, 97%, 97%, and 93%, respectively. Survival rate without myocardial infarction at 1, 3, 5, and 10 years was 86%, 85%, 83%, and 81%, respectively. By univarite analysis, ST segment elevation in both the anterior and inferior electrocardiographic leads was the most important factor influencing survival, followed by use of calcium antagonists, left ventricular function, smoking, and alcohol intake. The variables that significantly correlated with survival without myocardial infarction were use of calcium antagonists, left ventricular function, extent and severity of coronary artery disease, coronary artery bypass surgery, and disease activity. Multivariate analysis using the Cox proportional hazards model showed that intake of calcium antagonists, extent and severity of coronary artery disease, and ST segment elevation in both the anterior and inferior leads were significant independent predictors of survival without myocardial infarction. We conclude that long-term prognosis for patients with variant angina is relatively good and that use of calcium antagonists improves it.

In four patients with exertional angina induced by arm exercise, coronary arteriograms taken before, during and after the attack demonstrated that spasm appeared in the large coronary artery supplying the area of myocardium shown to be ischemic in the electrocardiogram during the attack. The spasm disappeared with subsidence of the attack after administration of nitroglycerin. Anginal attacks induced by treadmill exercise were not suppressed by propranolol, 60 mg orally, in two of the four patients. However, such attacks were suppressed in all patients by oral administration of diltiazem (90 mg, four patients) or nifedipine (20 mg, three patients) or intramuscular injection of phentolamine (0.2 mg/kg body weight, three patients). It is concluded that coronary arterial spasm can be induced by exercise and can cause exertional angina in some patients. Diltiazem and nifedipine, calcium antagonistic drugs, prevent spasm.

We retrospectively compared the efficacy of percutaneous transluminal coronary angioplasty (PTCA) and intracoronary thrombolysis (ICT) in patients with acute myocardial infarction (AMI). The ICT group consisted of 62 consecutive patients who underwent ICT before the introduction of PTCA for AMI and who were considered to be candidates for PTCA based on review of their cine-films. The PTCA group consisted of 92 consecutive patients who underwent PTCA thereafter. The reperfusion rate was significantly higher in the PTCA group than in the ICT group (92.4% vs 71.4%, p less than 0.01) and the residual stenosis was significantly lower in the former. Furthermore, the incidences of reinfarction and post-infarction angina were significantly lower in the former than in the latter (3.3% vs 12.9%, p less than 0.05 and 6.5% vs 29.0%, p less than 0.001 respectively). Although the degree of improvement in left ventricular function was influenced by the result of reperfusion, it was not affected by the reperfusion method. Therefore, PTCA did not improve left ventricular function more than ICT unless ICT alone failed to achieve reperfusion.

The relations of several creatine kinase (CK) variables to angiographic left ventricular ejection fraction and abnormally contracting segments in the chronic phase were examined in 2 groups of patients with a first anterior acute myocardial infarction. In group A (n = 22), emergency coronary angiography was performed and nonsurgical early reperfusion was attempted. Such an early revascularization, which was considered partially present in group B (n = 16), which received conventional therapy, shifted the CK time-activity curve to the left and altered its relation to angiographic cardiac function. At similar levels of peak CK, myocardial damage was significantly smaller in patients with successful thrombolysis than in those with unsuccessful reperfusion and conventional therapy (p less than 0.01). In patients whose infarct was considered to be moderate according to peak CK (1,000 to 3,000 U/liter), there was significant correlation between time to peak CK and left ventricular ejection fraction or percent abnormally contracting segments irrespective of their group. The results suggest that one should take into account rapid washout and shorter time to peak CK when estimating enzymatic infarct size in humans. The multivariate analysis of cardiac function with peak CK and time to peak CK resulted in a closer correlation in all patients. Such a correction in the time to peak CK may be a clinically useful approach for better interpretation of infarct size.

We gave alcohol to 15 patients with variant angina to induce the attacks at the hospital. Anginal attacks were repeatedly induced in seven of them. Although the time lag between alcohol ingestion and the attacks varied widely among patients, from 1.5 to 12 hours, it was fairly constant in each patient. We carefully examined the histories of 101 patients with variant angina to become familiar with the relationship between alcohol ingestion and the attacks of angina. Seventy-one patients took alcohol in their daily lives. Nineteen of the 71 patients (26.8%) who took alcohol had a definite relationship between alcohol ingestion and the attacks. We conclude that alcohol induces anginal attacks or coronary artery spasm in not a small number of patients with variant angina.

In 31 patients with transmural myocardial infarction in whom coronary arteriography was performed within 8 hours after the onset of symptoms, we examined (1) the effect of restoration of coronary blood flow on serum CPK time-activity curve and (2) the relationship between cumulative CPKr and the left ventricular function in the chronic phase. We divided 31 patients into 2 groups: Group A consists of 19 patients in whom coronary reperfusion was established. Group B consists of 12 patients whose coronary artery remained occluded. In group A, the time required to reach peak serum CPK activity was significantly shorter than in group B. When comparing CPKr with percent abnormally contracting segment (%ACS) in 2 groups, correlation between CPKr and %ACS was not good, but it revealed linear relation in both group A and B. CPKr divided by %ACS (CPKr/%ACS) was significantly higher in group A than in group B. We conclude that reperfusion of infarct-related coronary artery changes serum CPK time-activity curve resulting in earlier appearance of peak serum CPK and that infarct size cannot be estimated by serum CPK level alone.

We examined the effects of changes in pH, Ca2+ concentration, diltiazem, nitroglycerin, and propranolol on the vascular tone of the isolated rabbit coronary artery. Stepwise increase in pH of the bath fluid caused pH-dependent increased vascular tone. Increase in Ca2+ concentration of the bath fluid also resulted in increased vascular tone, while removal of Ca2+ abolished the high pH-induced elevated vascular tone. Diltiazem and nitroglycerin suppressed the high pH-induced increased vascular tone. Propranolol in high concentrations exhibited a direct inhibitory effect on the high pH-induced increased vascular tone. We conclude that high pH induces coronary vasoconstriction principally by increasing transmembrane influx of Ca2+ and that diltiazem and nitroglycerin suppress this action.