Minoru Hirota

Coronary pressure measurement to determine treatment strategy for equivocal left main coronary artery lesions

It is often hard to select a treatment strategy for equivocal left main coronary artery (LMCA) disease. We investigated the usefulness of coronary pressure (CP) measurement for determining the treatment strategy in intermediate LMCA disease. We measured CP in 15 consecutive patients with equivocal LMCA disease (age 67.6 ± 7.5 years, 14 males). Myocardial fractional flow reserve (FFRmyo) was obtained as the ratio of CP distal to the lesion/aortic pressure under maximal coronary dilation. Patients with FFRmyo ≥0.75 and <0.75 received medical therapy and coronary artery bypass grafting (CABG), respectively, and were followed up for 32.5 ± 9.7 (20–47) months. Eight patients received medical therapy and 7 patients underwent CABG in accordance with the FFRmyo criteria noted above. FFRmyo of the LMCA was 0.91 ± 0.01 and 0.61 ± 0.03 in patients who received medical and surgical therapy, respectively. Neither reference vessel diameter, minimal lumen diameter, nor percent diameter stenosis was significantly different between patients who received medical and surgical therapy. During the follow-up period, no patients with medical therapy showed symptoms due to the LMCA lesion. Similarly, 5 of 7 patients with CABG showed improvement of symptoms and the remaining 2 patients were hospitalized with congestive heart failure. No cardiac death was recorded in the patients with medical or surgical therapy. In conclusion, the present results clearly demonstrated that CP is clinically useful for determining the treatment strategy for equivocal LMCA lesions but coronary angiography is not.

Coronary pressure measurement to identify the lesion requiring percutaneous coronary intervention in equivocal tandem lesions.

ObjectivesNo reliable methods are available for determining application of percutaneous coronary intervention for treatment of equivocal tandem lesions. We investigated whether coronary pressure measurement is useful for determining the lesion that requires percutaneous coronary intervention in tandem lesions. MethodsWe measured coronary pressure in 72 consecutive patients with tandem lesions. Myocardial fractional flow reserve (FFRmyo) was obtained as the ratio of coronary pressure distal to the lesion/aortic pressure under maximal hyperemia. If the FFRmyo across the tandem lesions was ≥0.75, we deferred percutaneous coronary intervention for the lesion. When the tandem lesions showed FFRmyo<0.75, percutaneous coronary intervention was performed on the lesion that showed angiographically higher stenosis. When FFRmyo was <0.75 after one-lesion percutaneous coronary intervention, this intervention was carried out on the remaining lesion. ResultsWe deferred percutaneous coronary intervention for 26 patients (36.1%), and performed percutaneous coronary intervention in 46 patients (63.8%). We performed percutaneous coronary intervention for one lesion in 19 patients (26.4%) and for both lesions in 27 patients (37.5%). Among patients in whom percutaneous coronary intervention was deferred, only two patients (7.7%) required target lesion revascularization during the follow-up period. This rate was not higher than that in the 46 patients who underwent percutaneous coronary intervention for one or two lesions (six patients, 13.0%). Similarly, the target lesion revascularization in lesions with initially deferred percutaneous coronary intervention (5.6%, 4/71 lesions) was not higher than that in lesions with percutaneous coronary intervention (15.1%, 11/73 lesions). Major cardiac events, cardiac death and acute myocardial infarction, did not occur in patients with deferred percutaneous coronary intervention and in those with percutaneous coronary intervention during the follow-up period. ConclusionOur results clearly showed that coronary pressure measurement was clinically useful for identifying equivocal tandem lesions requiring percutaneous coronary intervention.

Relationship between activin A level and infarct size in patients with acute myocardial infarction undergoing successful primary coronary intervention.

BACKGROUND Activin A, a member of the transforming growth factor-beta cytokine family, has been suggested to have a role in inflammation. We examined the serum level of activin A in patients with acute myocardial infarction (AMI) undergoing successful primary percutaneous coronary intervention (PCI). METHODS The subjects were 30 AMI patients, 20 stable angina pectoris (AP) patients and 20 normal subjects. The serum levels of activin A in AMI patients were measured before PCI and on days 1, 2, 7, and 14. RESULTS Activin A levels before PCI in AMI patients (557+/-255 pg/ml) showed a significantly higher value than those in AP patients (364+/-159 pg/ml) and control subjects (316+/-144 pg/ml). Increased serum activin A level before PCI was decreased on day 2, and then gradually re-elevated on days 7 and 14. The serum activin A level before PCI was correlated with log-transformed peak creatine kinase (CK) as a surrogate of infarct size (r=0.48, p=0.008). Stepwise multiple regression analysis demonstrated that the serum activin A level before PCI was an independent predictor of peak CK. CONCLUSIONS The serum activin A level, increased in AMI, was positively correlated with peak CK and CK-MB levels which are measures of infarction size.

Single administration of vildagliptin attenuates postprandial hypertriglyceridemia and endothelial dysfunction in normoglycemic individuals

Postprandial hypertriglyceridemia impairs endothelial function and plays an important role in the development of atherosclerosis. The aim of the present study was to examine the postprandial effects of the dipeptidyl peptidase-4 inhibitor vildagliptin and the α-glucosidase inhibitor voglibose on endothelial dysfunction and lipid profiles following a single administration. A randomized cross-over trial using 11 normoglycemic individuals was performed. The postprandial effects of a single administration of vildagliptin (50 mg) or voglibose (0.3 mg) on endothelial function were analyzed using brachial artery flow-mediated dilation (FMD) and lipid profiles during fasting and 1.5 and 3 h after an oral cookie-loading test. Compared with voglibose, vildagliptin significantly suppressed postprandial endothelial dysfunction, (%FMD, −1.6±0.9 vildagliptin vs. −4.0±0.7 voglibose; P=0.01) and the postprandial incremental increase in the triglyceride level (28±18 vildagliptin vs. 51±26 mg/dl voglibose; P=0.01) 3 h after a cookie-loading test. In addition, vildagliptin significantly increased the levels of glucagon-like peptide-1 compared with voglibose 3 h after a loading cookie test (4.4±0.6 vs. 2.9±0.7 pmol/l, respectively; P=0.04). No significant differences in the levels of glucose, apolipoprotein B-48, glucagon or insulin were observed between vildagliptin and voglibose treatments. In conclusion, a single administration of vildagliptin attenuated postprandial endothelial dysfunction and postprandial hypertriglyceridemia, suggesting that vildagliptin may be a promising antiatherogenic agent.

Coronary Flow Reserve after Coronary Intervention is Similar in Patients with Preserved Viability in Previous Myocardial Infarction and in Those with Angina Pectoris

The relationship between coronary flow reserve (CFR) and viability in the infarcted myocardium has not been fully clarified. We measured coronary blood flow velocity immediately after coronary intervention (with percutaneous transluminal coronary angioplasty [PTCA] or stenting) in 38 patients with previous myocardial infarction and preserved viability and 48 with angina pectoris. CFR was calculated and was similar between the two patient groups. No differences in the incidence of post-intervention CFR > 2.0 were detected; there were no differences in postintervention CFR between patients with preserved myocardial viability and those with angina pectoris who underwent PTCA. Coronary stenting reduced the percentage diameter stenosis in both groups compared with PTCA and slightly increased the post-intervention CFR. No differences were, however, detected in postintervention CFR between patients with preserved myocardial viability and those with angina pectoris who underwent additional stenting. These results reveal that in patients with preserved myocardial viability, post-intervention CFR was restored to values similar to those in patients with angina pectoris.

Significant correlation of recruitable coronary collateral blood flow determined by coronary wedge pressure with ST-segment elevation during coronary occlusion.

ObjectivesQuantitative assessment of coronary collateral blood flow can be archived by measuring coronary pressure. We studied the relationships between recruitable coronary collateral blood flow and electrocardiographic changes during percutaneous coronary intervention (PCI). MethodsWe measured coronary pressure during coronary occlusion with PCI in 119 patients with left anterior descending coronary artery stenosis. During balloon inflation, the electrocardiogram was continuously recorded. The ST-segment elevation in the most elevated lead was defined as MaxST and the sum of the maximal ST elevation in leads V2–V4 was defined as ΣST. Fractional collateral flow (Qc/QN) was calculated as the coronary wedge pressure divided by the mean aortic pressure. Myocardial ischemia was defined as an ST-segment shift >0.1 mV in any of the V2, V3 or V4 leads. ResultsA significant relationship between Qc/QN and MaxST was observed (r=−0.455, P<0.0001). Similarly, Qc/QN was significantly correlated with ΣST (r=−0.477, P<0.0001). The receiver operating characteristic curve showed that a cut-off value of 0.27 for Qc/QN, with sensitivity of 71.4% and specificity of 76.2%, was an indicator of electrophysiologically sufficient recruitable coronary collateral blood flow for prevention of ischemia during coronary obstruction. Qc/QN values during the first, second, third and fourth inflation were not significantly different. ConclusionsQc/QN could be clinically useful for determining whether there is electrophysiologically sufficient recruitable coronary collateral blood flow for prevention of ischemia during coronary obstruction. Repeat transient coronary occlusion during PCI did not lead to increased collateral blood flow.