Left circumflex coronary artery is protected against no-reflow phenomenon following percutaneous coronary intervention for coronary artery disease.

Despite the positive impact of percutaneous coronary intervention (PCI) on reducing mortality, a small percentage of patients experience poor myocardial reperfusion following PCI. However, factors associated with no-reflow remain unclear. We investigated clinical factors associated with no-reflow following PCI for coronary artery disease (CAD). We retrospectively analyzed 1622 consecutive CAD patients who underwent PCI over a 5-year period at our institution. Patients were divided into two groups according to the presence (n = 31) or absence (n = 1591) of no-reflow, defined as Thrombolysis in Myocardial Infarction flow grade <3 after PCI. No significant differences in patient characteristics or PCI strategy were seen between the no-reflow and normal flow groups. The incidence of no-reflow was significantly lower in the left circumflex artery (LCx) than in the left anterior descending artery (LAD) (P = 0.0015), with no differences in characteristics or PCI strategy between these two target vessels. Multivariate analysis revealed that involvement of the LCx was an independent protective factor against no-reflow (odds ratio 0.14, 95 % confidence interval 0.02-0.98, P = 0.044). In conclusion, LCx as the target vessel was protective against no-reflow compared with LAD following PCI for CAD. Our results suggest that embolic protection devices may be unnecessary in CAD patients with involvement of LCx.

Provocation of microvessel spasm by low-dose acetylcholine in patients with suspected coronary artery disease--two case reports.

Endothelial dysfunction plays an important role in the pathogenesis of cardiac syndrome X, and intracoronary low-dose acetylcholine infusion is a widely used diagnostic modality for studying the coronary artery endothelial function. The authors herein report 2 cases of cardiac syndrome X with coronary artery endothelial dysfunction and microvessel spasm. The findings of non-invasive testing were positive for ischemia. Coronary angiograms appeared entirely normal in both cases. However, the intracoronary infusion of low-dose (1.5-15 microg/minute) acetylcholine demonstrated an impairment of the coronary blood flow response and consequently provoked an ST-segment elevation in an electrocardiogram. The coronary angiograms showed no spasm in the epicardial arteries. These patients are thus suggested to have cardiac syndrome X with microvessel spasms associated with coronary artery endothelial dysfunction.

Altered fractal behavior and heart rate variability in daily life in neurally mediated syncope.

Autonomic imbalance is thought to play an important role in the pathogenesis of neurally mediated syncope (NMS). Heart rate variability (HRV) indices and fractal dimension derived from 24 h ambulatory electrocardiogram (AECG) reflects the cardiac autonomic activity and provides useful information for understanding the pathogenesis of NMS. In this study, we sought the cardiac autonomic activity and the status of fractal dimension in daily life in patients with NMS. The 24 h ambulatory ECG recordings were performed in 36 NMS patients (NMS group) and in 11 healthy volunteers (CTRL group). Six time domain and frequency domain HRV indices were calculated. The regression of log (power) on log (frequency) was also calculated and the slope of the regression line (beta) was analyzed in three different periods such as total 24 h, awake and sleep phases. The values of mean RR, SDNN and SDANN were not significantly different, but the values of S.D. index, rMSSD, pNN50 and all the frequency domain HRV indices were significantly higher in NMS group than in CTRL group. For 24-h period, there was no significant difference in the values of beta. For awake phase, the value of beta was significantly higher in NMS group than in CTRL group. For sleep phase, the value of beta was significantly lower in NMS group than in CTRL group. Augmented autonomic activity and the deterioration of fractal dimension in daily life might contribute to the pathogenesis of NMS.

Sarpogrelate, a specific 5HT2-receptor antagonist, improves the coronary microcirculation in coronary artery disease.

BACKGROUND: Serotonin (5-hydroxytryptamine: 5-HT) reduces the coronary blood flow (CBF) as a product of aggregating platelets. Sarpogrelate, a specific 5HT2-receptor antagonist, has been reported to increase the coronary collateral flow in humans: however, its effect on the microcirculation is still not fully understood. HYPOTHESIS: This study was undertaken to determine whether sarpogrelate might improve the microcirculation in coronary artery disease (CAD). METHODS: To investigate the effect of sarpogrelate on the microcirculation in CAD, we measured CBF in 15 patients with CAD but no significant stenosis in the left anterior descending artery (LAD). The patients were randomly allocated to two groups, including those receiving oral administration of 200 mg of sarpogrelate (SPG, 8 patients, age 61 +/- 6 years) and those receiving no medication (controls, 7 patients, age 57 +/- 8 years). Prior to and 1 h after the administration of sarpogrelate, or in controls at 1-h intervals, the average peak velocity (APV) at baseline and hyperemia was measured by an intracoronary Doppler guidewire. Systemic blood pressure (SBP) and cardiac output (CO) were also measured. RESULTS: In the patients receiving SPG, the medication significantly increased the baseline (18 +/- 9 to 19 +/- 10 cm/s, p < 0.05) and maximal APV (55 +/- 9 to 64 +/- 31 cm/s, p<0.05). However, no significant changes were observed in SBP and CO after the administration of SPG. In the control group, there were no significant differences in baseline and hyperemic APV. CONCLUSION: Sarpogrelate increased both baseline and maximal CBF without changing the systemic hemodynamics. These findings thus support that SPG improves the microcirculation by antagonizing the vasoconstrictive products of the aggregating platelets in CAD.

[The mechanism of neurally mediated syncope assessed by an ambulatory radionuclide monitoring system and heart rate variability indices during head-up tilt].

PURPOSE: Previously, we tested the hypothesis that the great decline in left ventricular volume during head-up tilt test could trigger ventricular mechano-receptor activation, using ambulatory radionuclide monitoring system (C-VEST system). The aim of this study is to investigate the mechanism of tilt-induced syncope further, based on our previous report. METHOD: We measured the temporal changes in left ventricular volume, ejection fraction, cardiac output, and heart rate variability indices during head-up tilt test in 34 patients with syncope of an underdetermined etiology. RESULT: Twenty-two patients had a positive response (P group). Twelve patients showed a negative response (N group). Before syncope, left ventricular volume declined (P group, diastolic volume; -7.9 +/- 6.8%: systolic volume; -23.3 +/- 33.8%: N group, diastolic volume; -2.5 +/- 1.9%: systolic volume; 0.6 +/- 9.5%: p < 0.05), ejection fraction increased (P group, 3.9 +/- 2.5%; N group, -3.5 +/- 7.2%; p < 0.005), and high frequency spectra increased (P group, 12.0 +/- 20.3%; N group, 3.1 +/- 9.7%; p < 0.05), more extremely in the P group than in the N group. The value of the high frequency spectra before the head-up tilt test was significantly higher in the P group than in the N group (P group, 5.8 +/- 0.9 ms; N group, 5.0 +/- 1.1 ms; p < 0.05). CONCLUSIONS: (1) The precise evaluation of left ventricular volume by ambulatory radionuclide monitoring system combined with a heart rate variability analysis is considered to be useful for clarifying the pathophysiology of neurally mediated syncope. (2) Patients with neurally mediated syncope have higher baseline parasympathetic tone than normal population.

A case of transient mid-ventricular akinesia (a variant form of Takotsubo cardiomyopathy) followed with I-123-beta-metyl-iodophenyl pentadecanoic acid and I-123-meta-iodobenzyl-guanidine myocardial scintigraphy.

A 67-year-old woman without history of heart disease was admitted with chest oppression. Her electrocardiogram (ECG) at the time of admission showed ST segment elevation in leads V2-V6. Cardiac ultrasound revealed severe hypokinesis in mid to apical portion of anterior wall. Emergent coronary angiography showed normal coronary arteries. Left ventriculography (LVG) revealed akinesis of mid portion of anterior and inferior wall with hyperkinesis of apex and basal portion of anterior and inferior wall. Cardiac ultrasound examination 3 months later revealed improvement in LV contraction without mid-ventricular akisesia. The LVG performed 6 months later showed no focal asynergy. In I-123-beta-metyl-iodophenyl pentadecanoic acid myocardial scintigraphy the discrepancy of uptake between apical and anterior and inferior wall of mid region (more uptake in apex) was reduced. Using I-123-meta-iodobenzyl-guanidine myocardial scintigraphy in acute phase, decreased uptake in the mid portion of anterior and inferior to lateral wall was seen in early and delayed images and that persisted through 6 months. As these findings resembled those of Takotsubo cardiomyopathy other than affected region, it is possible to say that basically they belong to same entity of disease but they are different in their phenotype.