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Background An association between uric acid (UA) and cardiovascular diseases, including heart failure (HF), has been reported. However, whether UA is a causal risk factor for HF is controversial. In particular, the prognostic value of lowering UA in patients with HF with preserved ejection fraction (HFpEF) is unclear. Methods and Results We enrolled patients with HFpEF from the PURSUIT‐HFpEF (Prospective Multicenter Observational Study of Patients With Heart Failure With Preserved Ejection Fraction) registry. We investigated whether UA was correlated with the composite events, including all‐cause mortality and HF rehospitalization, in patients with hyperuricemia and HFpEF (UA >7.0 mg/dL). Additionally, we evaluated whether lowering UA for 1 year (≥1.0 mg/dL) in them reduced mortality or HF rehospitalization. We finally analyzed 464 patients with hyperuricemia. In multivariable Cox regression analysis, UA was an independent determinant of composite death and rehospitalization (hazard ratio [HR], 1.15 [95% CI, 1.03–1.27], P =0.015). We divided them into groups with severe and mild hyperuricemia according to median estimated value of serum UA (8.3 mg/dL). Cox proportional hazards models revealed the incidence of all‐cause mortality was significantly higher in the group with severe hyperuricemia than in the group with mild hyperuricemia (HR, 1.73 [95% CI, 1.19–2.25], P =0.004). The incidence of all‐cause mortality was significantly decreased in the group with lowering UA compared with the group with nonlowering UA (HR, 1.71 [95% CI, 1.02–2.86], P =0.041). The incidence of urate‐lowering therapy tended to be higher in the group with lowering UA than in the group with nonlowering UA (34.9% versus 24.6%, P =0.06). Conclusions UA is a predictor for the composite of all‐cause death and HF rehospitalization in patients with hyperuricemia and HFpEF. In these patients, lowering UA, including the use of urate‐lowering therapy, may improve prognosis.

Background The method to perform a precise mapping of non-pulmonary vein (PV) triggers has not been fully investigated. The purpose of this study was to assess the efficacy of self-reference mapping for eliminating non-PV triggers in a large series of patients including the long-term outcomes. Method Among 446 atrial fibrillation (AF) ablation procedures in 431 patients at 2 institutions, we prospectively enrolled patients who had reproducible non-PV triggers. Non-PV triggers from the left atrial posterior wall (LAPW) and superior vena cava (SVC) were excluded. Ablation procedure and long-term clinical outcomes were evaluated. The origin of non-PV triggers were detected using a self-reference mapping technique, which does not require any other reference catheters. Instead of using signals obtained from a fixed intracardiac catheter as the reference, an operator repeatedly moved a multi-electrode catheter to the earliest site creating a new reference each time to map the non-PV trigger. Results A total of 32 non-PV triggers excluding origins from the LAPW and SVC were induced in 23 patients. All triggers were mapped using a self-reference mapping technique with 11.0 ± 10.2 min and eliminated by radiofrequency ablation with 10.7 ± 10.0 points application. No major complications were observed. During the follow-up (529 ± 270 days), 18 patients (77%) were free from atrial tachyarrhythmias after a 3-month blanking period. Three patients received additional ablation procedures. No non-PV triggers ablated during the previous procedure were observed. Conclusions A novel self-reference mapping technique is useful for eliminating non-PV triggers for the short- and long-term outcomes.

A 42‐year‐old woman without a history of catheter ablation or cardiac surgery was referred to our institution for a paroxysmal atrial tachycardia (AT). Programed stimulation could not induce any AT. The AT spontaneously initiated during a continuous isoproterenol infusion. The earliest activation during the AT was recorded at the cavo‐tricuspid isthmus, and local abnormal atrial activity (LAATA) was recorded during sinus rhythm at that same site. When rapid atrial activity was recorded at the cavo‐tricuspid isthmus where the LAATA was recorded, an AT was induced. Radiofrequency ablation was performed over the entire area where the LAATA was recorded during sinus rhythm, rendering the AT non‐inducible.

A 69-year-old woman with palpitations was referred to our hospital for a second session of atrial fibrillation (AF) catheter ablation. She had a history of AF ablation including pulmonary vein (PV) isolation and persistent left superior vena cava (PLSVC) isolation. Electrophysiologic studies showed the veno-atrial connections that had recovered. After PV isolation was performed, AF was induced by atrial premature contraction (APC) from the PLSVC, and AF storm occurred. During PLSVC isolation, AF was not induced by APC from the PLSVC. PLSVC isolation continued during sinus rhythm. The elimination of the PLSVC potential was difficult to confirm because of the far-field potential of the left ventricle. Then, we performed right ventricular pacing. The remaining PLSVC potential was identified. After that, the PLSVC isolation was successful during right ventricular pacing. Complications were not observed. The patient had no recurrence of AF thereafter. Keywords: Persistent left superior vena cava, Atrial fibrillation, Catheter ablation, Ventricular pacing, Non-pulmonary vein foci

A 76-year-old man presented with frequent premature ventricular contractions (PVCs). The electrophysiological findings revealed the origin of the PVCs was in the posterior-superior process of the left ventricle (PSP-LV), which is anatomically adjacent to the infero-medial aspect of the right atrium (RA). After a failed ablation from the LV, ablation in the RA eliminated the PVCs. During additional ablation, the atrio-his (AH) interval was monitored by atrial overdrive pacing, and ablation was terminated immediately after the AH interval prolonged to 174 ms. We believe that the atrial overdrive pacing was useful for monitoring the AH interval to prevent atrioventricular block during ablation of PVCs from the PSP-LV.

Late morbidity and death as a result of progressive coronary vascular obliteration remains a major unsolved problem after orthotopic heart transplantation. Various percutaneous catheter intervention (PCI) methods have been used to treat transplant coronary artery disease (CAD), but few reports have assessed the longitudinal results of these procedures. Of 1,440 cardiac transplant patients at University of California, Los Angeles, Medical Center, treated between 1984 and 2004, 65 patients who had undergone orthotopic heart transplantation underwent PCI on a total of 156 coronary artery lesions because of transplant CAD between July 1993 and August 2004. The procedural success rate was 93%. Angiographic follow-up was available for 42 patients and 101 lesions 9.5 +/- 5.8 months after PCI. The global restenosis rate was 36%. Multivariate analysis was used to assess 49 clinical, angiographic, and immunologic variables per lesion. The use of a cutting balloon increased the risk of restenosis (odds ratio 11.5, p

Transplant vasculopathy significantly limits the survival of cardiac transplant patients and occurs in 50% of patients by 5 years posttransplant. We report our experience with six cardiac transplant patients who underwent intracoronary brachytherapy for in-stent restenosis. At four centers, six patients underwent intracoronary radiation for in-stent restenosis. All patients received extended antiplatelet therapy with clopidogrel and aspirin. Follow-up angiography was performed in all patients. Two of the six patients underwent subsequent target lesion revascularization. Patient 1 presented with total occlusion of her radiated lesion. She had a complex procedure requiring stenting for a dissection after the radiation dwell. Patient 2 had high-grade restenosis following brachytherapy. Patient 3 had a 50% restenotic lesion. Patients 4, 5, and 6 had follow-up angiography that showed no evidence of restenosis. There are few good options to treated accelerated transplant vasculopathy. Radiation therapy may be a viable option in this difficult patient population.

Subacute stent thrombosis occurred in a patient 34 days after receiving a heparin-coated (HC) stent. The patient developed heparin-induced thrombocytopenia and diffuse thrombosis after the stent was placed. This raises the concern that patients who develop heparin-associated antibodies in the context of a recently placed HC stent may have an increased risk for subacute stent thrombosis.

We performed Cutting Balloon angioplasty on 20 lesions in 11 heart transplant recipients 7.5 +/- 3.8 years after transplantation. The mean percentage of diameter stenosis decreased from 88.3% +/- 13.8% to 19.6% +/- 13.7% after Cutting Balloon angioplasty without complication. Seven patients underwent follow-up angiography at 4.9 +/- 1.7 months in a total of 12 lesions, and all lesions showed restenosis with a mean diameter stenosis of 84.4% +/- 19.2%. Cutting Balloon angioplasty can be used to treat obstructions in cardiac transplant coronary arteries; however, it may cause exacerbation and produce a high restenosis rate.

OBJECTIVES: The purpose of this study was to assess whether the newer stent delivery systems provide a stented lumen cross-sectional area (CSA) that is equal to the delivery balloon nominal dimensions. BACKGROUND: First generation stents were often not adequately expanded with their delivery system and frequently required higher pressure or a larger balloon after deployment. Newer stents were designed to optimize expansion with noncompliant, high-pressure balloons provided as the delivery systems. METHODS: Intravascular ultrasound (IVUS) was used to evaluate 38 stents in 32 patients after deployment at 14 to 16 atm with their delivery balloon system. Minimum stent lumen CSA and stent minimum lumen diameter (MLD) were measured by IVUS imaging. The manufacturer's expected stent diameter was defined as the balloon diameter measured by the company at the maximum pressure used. The manufacturer's expected stent area was calculated based on the manufacturer's expected stent diameter. RESULTS: The MLD (2.5 +/- 0.5 mm) and minimum stent CSA (6.0 +/- 1.7 mm(2)) by IVUS were significantly smaller than the manufacturer's expected stent diameter (3.5 +/- 0.4 mm) and area (9.5 +/- 1.9 mm(2)) (p < 0.0001, respectively). The mean MLD by IVUS was 72 +/- 8% of the expected stent diameter, and the mean minimum stent CSA by IVUS was 62 +/- 10% of the expected stent area. CONCLUSIONS: Despite moderately high-pressure inflations, the mean minimum stent CSA actually achieved was, on average, only 62% of the manufacturer's expected stent area. To optimize stent deployment, these IVUS observations should be considered during coronary artery stenting.

The present study seeks to estimate the difference between coronary zero flow pressure (Pzf) by analysis of the baseline pressure - flow relationship and the Pzf calculated during a long diastole in humans. Although Pzf is likely to provide meaningful information about the characteristics of coronary circulation, there are no available data on Pzf in humans because Pzf is overestimated when it is calculated during normal cardiac cycles. Actual Pzf was determined in 15 subjects by analyzing the coronary pressure - flow relationship during a long cardiac cycle induced by an intracoronary adenosine triphosphate (ATP) infusion, and it was compared with the Pzf calculated during a normal cardiac cycle in order to estimate the difference. Pzf calculated during a normal cardiac cycle was 47±15 mmHg, which decreased to 36±9 mmHg after intracoronary administration of ATP (0.05 mg) whereas actual Pzf was 21±7 mmHg. Pzf calculated in a pressure - flow relationship during a normal cardiac cycle under vasodilation correlated well with that during a long diastole (r=0.75, p

The left ventricle's morphological adaptation to high blood pressure is classified into 4 patterns based on mass and wall thickness. The geometric changes caused by maladaptation to pressure overload possibly relate to progression of contractile dysfunction with abnormal energy metabolism. The present study assessed whether the geometric adaptation of the left ventricle (LV) to high blood pressure relates to changes in myocardial energy metabolism, especially free fatty acid (FFA) utilization. Thirty-five patients with essential hypertension underwent echocardiography and dual isotopes myocardial scintigraphy using iodine-123 labeled 15-p-iodophenyl-3-(R,S)-methylpentadecanoic acid (BMIPP, an analogue of a FFA) and thallium-201 (Tl-201). Systolic (endocardial fractional shortening; %FS) and diastolic indices (the ratio of early to atrial filling waves; E/A) of LV function were also assessed. Quantitative myocardial BMIPP uptake was evaluated by the BMIPP/Tl-201 myocardial uptake ratio (B/T). The subjects were divided into 4 groups based on LV mass and wall thickness: (1) concentric hypertrophy (CH), (2) eccentric hypertrophy (EH), (3) concentric remodeling (CR), and (4) normal geometry (N). The %FS was lower in the EH group than in the other groups. The mitral E/A ratio in the CH group was lowest. B/T was significantly decreased in the EH group compared with the N group (p

The purpose of this study was to assess the role of the autonomic nervous system in the regulation of basal coronary artery tone in normal and atherosclerotic plaque segments by using intravascular ultrasound in humans. In each of 21 patients, a short-axis image at one site of coronary artery was imaged by means of a 3.2F, 30-MHz intravascular ultrasound before and after intracoronary administration of 2 mg isosorbide dinitrate (ISDN). The authors identified the perimeters of the vessel wall segments with normal or atherosclerotic plaque on ultrasound images and evaluated the basal tone in each segment as a percent increase in each perimeter produced by ISDN. Using heart rate variability analysis for 512 seconds recorded immediately before ISDN administration, they evaluated cardiac sympathetic and vagal activities at rest as the integrated power of fast Fourier transform (FFT) spectrum for the low-frequency (LF: 0.04 to 0.15 Hz), and high-frequency (HF: 0.15 to 0.4 Hz) components, respectively. Of 29 segments examined by ultrasound, 16 were normal and 13 were atherosclerotic plaque. In all 29 segments, ISDN produced an increase in the perimeter of the vessel wall. At the normal 16 segments, the increase in perimeter by ISDN exhibited a significant correlation to the power of HF (r = 0.749, p = 0.0008) but no significant correlation to LF. At 13 plaque segments, however, no significant correlation between the response to ISDN and autonomic nerve activity was observed. In conclusion, the basal tone of normal coronary arterial wall segment is closely related to parasympathetic nerve, whereas the relation is impaired in mild atherosclerotic segments.

Adenosine triphosphate (ATP) is reported to be released mainly from presynaptic vesicles and cardiomyocytes. The released ATP, which can be degraded to adenosine, may cause coronary vasodilation. However, there is no clear evidence that ATP is degraded to adenosine and causes coronary vasodilation in humans. The present study was undertaken to test whether intracoronary administration of ATP increases myocardial adenosine levels and coronary blood flow. In 11 patients, 3 doses of ATP (0.1, 0.2, and 0.4 mg) were injected into the left anterior descending coronary artery. The velocity of coronary blood flow was measured by Doppler flow probe, and the adenosine concentration in the coronary sinus blood was measured. We also continuously infused ATP (0.2 mg/min) for 1 min in another 10 patients. Coronary blood flow increased dose dependently soon after injection of ATP, Coronary arteriovenous differences in adenosine concentration increased [from 21±15 to 178±15 pmol/ml (p

OBJECTIVE To elucidate whether impairment of the myocardial free fatty acid (FFA)metabolism and small vessel abnormalities in the myocardium are etiologic or contributory factors of myocardial dysfunction in patients with NIDDM without any significant coronary artery disease RESEARCH DESIGN AND METHODS We performed myocardial imaging with 123I-labeled β-methyl-p-iodophenyl pentadecanoic acid (BMIPP), a branched analog of FFA, and dipyridamole-infusion 201 thallium scintigraphy (Dip) in nine patients who demonstrated left ventricular wall motion abnormalities without any significant coronary artery disease and in fifteen control cases. As an index of myocardial FFA metabolism, the heart-to-mediastinum count ratio (H/M) of BMIPP was calculated from the mean count in the regions of interest at the heart and the upper mediastinum RESULTS Nine patients with reduced wall motion documented by left ventriculography (LVG) (hypokinetic group) demonstrated significantly lower BMIPP uptake (2.1 ± 0.2, mean ± SD) than fifteen patients with normal wall motion (normokinetic group) (2.3 ± 0.2, P CONCLUSIONS Our findings suggest that impairment of myocardial FFA metabolism rather than small vessel abnormalities in the myocardium is responsible for modest left ventricular dysfunction in patients with diabetes

We report a case of hypertensive-diabetic cardiomyopathy demonstrating left ventricular regional wall motion abnormality, with a normal coronary artery documented on coronary arteriography. Dipyridamole-infusion 201Tl scintigraphy demonstrated transient perfusion defects in the infero-posterior wall of the left ventricle, where reduced wall motion was demonstrated on contrast left ventriculography. Myocardial SPECT (single photon emission tomography) imaging with [123I] β-methyliodophenylpentadecanoic acid (BMIPP) and 201Tl demonstrated reduced [123I]BMIPP uptake compared with 201Tl uptake in the infero-posterior wall of left ventricle. These results suggest that the impairment of myocardial free fatty acid metabolism is an etiologic or contributory factor for regional wall motion abnormality, together with small-vessel coronary artery disease, in this patient.