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Key Clinical Message The present case demonstrated a rare situation alternating between a repetitive atrial tachycardia (AT) and ventricular tachycardia (VT). A unique induction mechanism was noted in which the VT was induced after Wenckebach AV node conduction block following the repetitive rapid AT.

Background The clinical relevance of examining human atrial natriuretic peptide (HANP) or left atrial appendage (LAA) wall-motion velocity during sinus rhythm in paroxysmal atrial fibrillation (AF) patients has not been clearly elucidated. Methods The subjects were 38 patients with paroxysmal AF who underwent transesophageal and transthoracic echocardiography during sinus rhythm. The presence of spontaneous echocontrast (SEC) was examined with transesophageal echocardiography and LAA wall-motion velocity (LAAWV) was measured with transthoracic tissue Doppler echocardiography. Plasma HANP was measured within 3 hours after echocardiography. Results Human atrial natriuretic peptide ranged from 12 to 106 pg/mL with an average of 43 ± 24 pg/mL and had a significant correlation with LAAWV (r = −0.57) or LAA flow velocity (r = −0.41). HANP was significantly higher in patients with SEC than in patients without SEC (64 ± 29 vs. 34 ± 15 pg/mL, P = 0.008) and LAAWV was significantly lower in patients with SEC than in patients without SEC (13 ± 5 vs. 20 ± 5 cm/sec, P = 0.002). HANP >44 pg/mL had a sensitivity of 73% and specificity of 89% for diagnosing SEC. SEC was more frequently observed (73%) in patients with HANP >44 pg/mL and/or LAAWV

A 68-year-old woman exhibited an increasingly protruding mass on the left heart border on chest X-ray. Transthoracic echocardiography revealed an echo-free mass in the anterior pericardial space. Transesophageal echocardiography revealed blood flow from the proximal left anterior descending coronary into a large coronary artery aneurysm measuring 61 mm × 51 mm in diameter and a quadricuspid aortic valve with a small cusp between the left and right coronary cusps. Coronary angiography demonstrated the presence of a coronary aneurysm connected to the proximal left coronary anterior descending artery. A giant coronary artery aneurysm and pulmonary artery fistulas extending from the left and right coronary arteries were confirmed by surgeons and successfully treated with surgery.

Aims To investigate the clinical outcomes of paclitaxel-eluting stents (PES) and sirolimus-eluting stents (SES) in patients on dialysis. Methods and results Between May 2004 and December 2008, 95 patients on dialysis with 124 lesions were treated with PES alone, and were compared to 184 patients on dialysis with 244 lesions treated with SES alone, retrospectively. One-year major adverse cardiac event (MACE) including stent thrombosis, target lesion revascularisation (TLR), myocardial infarction (MI) and cardiac death were compared. Baseline characteristics were similar except for previous CABG (p = 0.02) and reference vessel diameter (p = 0.04). During hospitalisation, all cause death was more frequently observed in the PES group (p = 0.004). In-hospital MACE was not significantly different (p = 0.8). The incidence of 1-year MACE in the PES group was lower than that in the SES group (14.7%, 28.3%, p = 0.04), mainly due to the reduction of TLR (11.6%, 25.0%, p = 0.03). Rates of stent thrombosis (0%, 2.7%, p = 0.1), MI (1.1%, 3.8%, p = 0.2), and cardiac death (3.2%, 4.4%, p = 0.6) were not significantly different. Conclusions PES appears to be more efficient in reducing angiographic and clinical restenosis in dialysis patients compared with SES.

SummaryStenosis of the left main coronary artery (LMCA) due to extrinsic compression, producing symptoms of myocardial ischemia, is called left main compression syndrome. We report on a 43-year-old male with acute coronary syndrome who developed left main compression syndrome while waiting for a lung transplantation secondary to interstitial pneumonia, but underwent successful LMCA stenting as emergent treatment. Coronary angiography 3 months after the operation showed good stent patency in the LMCA, and the clinical course was favorable.

Background It is unknown whether adenosine triphosphate disodium (ATP) administration during primary percutaneous coronary intervention (PCI) is useful in anterior acute myocardial infarction (AMI). Methods The study was a prospective, non-randomized, open-label trial. Primary PCI was successfully performed in 204 consecutive patients with first anterior AMI. ATP at a mean dose of 117 μg/kg/min for 45 min on an average was infused intravenously during PCI in 100 patients (Group 1). In the other 104 patients, normal saline was administered (Group 2). ST-segment resolution (STR) was estimated 90 min after recanalization. The no-reflow ratio was measured 2 weeks later, using intravenous myocardial contrast echocardiography. Left ventricular ejection fraction (LVEF), LV regional wall motion (LVRWM), and LV end-diastolic volume index (LVEDVI) were measured 6 months later. Results Baseline patient characteristics of the two groups were similar, including TIMI risk scores. Significant STR (≧50% resolution compared to baseline) (66% versus 50%; Group 1 versus Group 2, p =0.02), no-reflow ratio (24% versus 34%, indicated by mean values, p =0.02), LVEF (61% versus 55%, p =0.0007), LVRWM (−1.56 versus −2.05, using the SD/chord, p =0.0001), and LVEDVI (60 ml/m 2 versus 71 ml/m 2 , p =0.0007) were significantly better in Group 1, and the no-reflow ratio, LVEF, LVRWM and LVEDVI were significantly better in ATP-administered patients, regardless of antecedent angina or advanced age. ATP Administration was consistently identified as a significant determinant for STR, no-reflow ratio, LVEF, LVRWM, and LVEDVI. Conclusions Intravenous ATP administration during reperfusion is an independent determinant of STR and the no-reflow ratio, and LVEF, LVRWM, and LVEDVI at 6 months after primary PCI.

Summary Background and purpose Administration of adenosine attenuates myocardial stunning after reperfusion in a canine experimental ischemic model. However, it is unknown whether administration of adenosine triphosphate disodium (ATP) during reperfusion can attenuate myocardial stunning after coronary recanalization in patients with acute myocardial infarction (MI). Therefore, we sought to elucidate the effects of ATP administration on serial changes of left ventricular systolic function before and after coronary recanalization. Methods In 27 patients with first ST-elevation acute anterior MI, in whom primary percutaneous coronary intervention (PCI) was completed within 10 h after symptom onset, ATP at a mean rate of 103 μg/kg/min (n = 16) or normal saline (n = 11) was intravenously administered for 1 h during reperfusion. Left ventricular regional wall motion within the initially severely ischemic region was serially analyzed using the standard wall motion score index (WMSI) by transthoracic echocardiography. Results Means of WMSIs were similar shortly before primary PCI in both groups (2.79 in ATP group and 2.69 in controls). They changed to 2.56 and 2.22 shortly after PCI, 2.49 and 2.39 on day 2, 2.34 and 2.30 on day 3, 2.19 and 2.25 on day 10, and 1.85 and 2.02, 6 months later, respectively. Transient improved regional wall motion within the initially severely ischemic region was observed shortly after PCI in controls (10.3% of observed segments); however, it was significantly suppressed in the ATP group (2.55%). The percent recovery of WMSI on day 10, which was defined as WMSI on day 10 normalized by improvement of WMSI for 6 months, was 63.8% in ATP group and 65.7% in controls, implying ATP administration could not reduce myocardial stunning by day 10 after primary PCI. Conclusions The high-dose administration of ATP during primary PCI prevented transient improved wall motion shortly after coronary recanalization rather than preventing left ventricular stunning. These results suggest that ATP can prevent reperfusion injury during primary PCI.

This study examined the role of left atrial (LA) appendage wall velocity (LAAWV) measurement in addition to LA size for the noninvasive assessment of thrombogenesis in patients with atrial fibrillation (AF) and normal plasma D-dimer levels.In 58 non-valvular AF patients, LAAWV and the LA volume index (LAVI) were determined by transthoracic echocardiography. LA appendage flow velocity and severity of spontaneous echo contrast (SEC) were determined by transesophageal echocardiography.LAAWV was strongly correlated with LA appendage flow velocity (r = 0.82), and LAVI was weakly correlated with LA appendage flow velocity (r = -0.37). As SEC severity increased, LAAWV decreased (p0.001) and LAVI increased (p0.001). Among 52 patients with normal D-dimer levels, LAAWV10 cm/s had 71 % sensitivity and 94 % specificity for diagnosing severe SEC. Severe SEC was not found in 18/32 large LAVI patients (34 mL/m(2)), but 17 of the 18 patients (94 %) had LAAWV10 cm/s. Severe SEC was found in 3/20 patients with normal LAVI, but all of them showed LAAWV10 cm/s.The noninvasive measurement of transthoracic LAAWV in addition to LA volume is clinically relevant for quantitatively assessing thrombogenesis in AF patients with normal D-dimer levels.

ObjectivesThe purpose of this study was to determine the relationship between matrix metalloproteinases (MMPs)-1, -2, and -9, and tissue inhibitors of metalloproteinases (TIMP)-1 and the atrial structural remodeling during atrial fibrillation (AF).BackgroundMatrix metalloproteinases, a family of proteolytic enzymes and TIMPs, regulate the extracellular matrix turnover in cardiac tissue.MethodsTissue samples were obtained from 25 patients without a history of AF (regular sinus rhythm [RSR]) and 13 patients with AF (paroxysmal AF: 6, chronic AF 7) undergoing cardiac operations. We performed a western blotting analysis of the MMP-1, -2, and -9, and quantitatively analyzed the expression of the MMP-9 and TIMP-1 by real time polymerase chain reaction and ELISA. The localization of the MMP-9 was investigated by in situ zymography and immunohistochemistry.ResultsThe active form of the MMP-9 was significantly increased in the AF group in comparison to that in the RSR group (p < 0.05), but there were no differences between the groups in the protein level of the latent form of the MMP-9 and active and latent forms of the MMP-1 and MMP-2. We also demonstrated that the expression of the MMP-9 was significantly more increased in the atria of the AF group than in that of the RSR group for both the messenger ribonucleic acid (mRNA) (AF: RSR; 1: 1.5) and protein levels (AF: RSR; 3.9 ± 1.3 : 1.5 ± 0.4 ng/mg atrium). The expression level of the MMP-9 was also higher in the PAF group than in the RSR group, however, the diameter of the left atrium was similar in both groups. The gelatinase activity and left atrium diameter were positively correlated (p < 0.05, R = 0.766). The relative expression of the mRNA for the monocyte chemoattractant protein-1 was higher in the AF group than in the RSR group. Immunohistochemical analysis revealed that the MMP-9 was distributed within the perivascular area and under the epicardium of the atria.ConclusionsWe clearly showed that the expression of the MMP-9 increased in fibrillating atrial tissue, which may have contributed to the atrial structural remodeling and atrial dilatation during AF.

Background: Myocardial bridging (MB) has been associated with cardiac events. Whether coronary spasm is one factor contributing to those events is unknown. Hypothesis: This study investigated whether the likelihood of coronary spasm is increased in patients with MB. Methods: A spasm-provocation test was performed by infusing acetylcholine into the left coronary artery in 114 Japanese patients with chest pain. The test result was defined as positive when the diameter of the coronary artery was reduced by > 50% and ST-segment changes were documented. Myocardial bridging was defined as a > 15% reduction in coronary arterial diameter during systole after intracoronary injection of nitroglycerin. Results: Myocardial bridging was identified in 41 patients (36%) and was located in the mid-segment of the left anterior descending coronary artery (LAD) in all patients. Patients with MB experienced coronary spasm more frequently than patients without MB (MB+: 73%; MB —: 40%, p = 0.0006). Furthermore, among patients with a positive spasm-provocation test, coronary spasm occurred more frequently in the midsegment of the LAD in patients with MB than in those without MB (MB+: 73%; MB — : 45%, p = 0.0259). Multivariate regression analysis demonstrated that MB was a predictor of coronary spasm (odds ratio: 3.478, p = 0.0088). Conclusions: These results suggest that MB increases the risk of coronary spasm and that coronary spasm may be the proximate etiology of cardiac events associated with MB.

It is not known if QT dispersion is useful for detecting coronary artery disease. We investigated whether QT dispersion at baseline and during adenosine triphosphate (ATP) infusion correlate with the imaging patterns obtained from ATP stress thallium-201 single-photon emission computed tomography (ATP-SPECT). QT dispersion was determined in 169 patients who underwent ATP-SPECT from 12-lead electrocardiograms obtained at baseline and 3 minutes after the beginning of ATP infusion. Based on the results of ATP-SPECT, patients were divided into 4 groups: normal (n = 55), ischemia (n = 38), ischemia and scar (n = 42), and scar (n = 34). Baseline QT dispersions (mean +/- SD) in the normal, ischemia, ischemia and scar, and scar groups were 48 +/- 15, 50 +/- 17, 69 +/- 25, and 70 +/- 24 ms, respectively. Baseline QT dispersion was significantly greater in the groups with myocardial scar. QT dispersions during ATP infusion were 43 +/- 16, 63 +/- 20, 76 +/- 20, and 62 +/- 25 ms in the normal, ischemia, ischemia and scar, and scar groups, respectively. QT dispersion increased with ATP infusion in patients with myocardial ischemia. QT dispersion at baseline and during ATP infusion correlated with the ATP-SPECT imaging pattern. These findings suggest that baseline QT dispersion and ATP-induced changes in QT dispersion may help detect the presence of myocardial ischemia and scar.

先天性QT延長症候群 (LQTS) 4例と対照群4例で, 右心室および左心室の2～3ケ所より単相性活動電位 (MAP) を同時記録し, 右房ペーシングで突然心周期を短縮させ, その前後の各心拍におけるMAPD90と, 再分極時間 (repolarization time) のばらつき (RT dispersion: RTの最長部位と最短部位の差) を計測した.LQTSでは, 心周期短縮前後を通して, MAPD90, RT dispersionは, 対照群より大きかった.両群とも心周期短縮後, 最初の数十拍で急速に短縮し, その後は数分かけて徐々に定常状態となった.LQTSでは心周期短縮後に心拍毎の変動を認めた.特に心周期短縮後早期にその傾向は強かった.LQTSにおける, 突然の心周期短縮に対する再分極過程の不安定さを反映するものと考えられた.また, 持続的な心周期短縮によりMAPD90, RT dispersionともに小さくなり, 再分極異常を改善させた.このことは, ペースメーカー治療の有効性を支持する結果と考えられた.

Left ventricular function and prognosis were evaluated in patients with acute myocardial infarction who underwent primary percutaneous coronary intervention supported by intraaortic balloon pumping.Fifty-eight consecutive patients with first acute myocardial infarction were treated between July 1999 and April 2006. Twenty-five had cardiogenic shock on admission, whereas 33 did not. Patients with anterior acute myocardial infarction without cardiogenic shock were divided into the prophylactic intraaortic balloon pumping group (Group 1; n=17) and the rescue intraaortic balloon pumping group (Group 2; n=9).Thirty-day in-hospital mortality was 52% in cardiogenic shock patients, and 3% in non-shock patients. Baseline characteristics of non-shock anterior acute myocardial infarction were similar including Thrombolysis in Myocardial Infarction (TIMI) risk scores (5.1 and 5.0) in the two groups. However, average left ventricular ejection fraction in the convalescent stage was superior in Group 1 (48.7% vs. 37.8%, p = 0.03). Thirty-day in-hospital mortality was 0% in Group 1 and 11% in Group 2 (p = 0.34). Cox's hazard ratio in Group 2 to Group 1 was 2.38 (95% confidence intrerval; 0.84-11.1, p = 0.09) in terms of the subsequent major cardiac events.Prophylactic use of intraaortic balloon pumping starting prior to primary percutaneous coronary intervention preserves the convalescent left ventricular systolic function in patients with high risk for anticipated cardiac events after anterior acute myocardial infarction without cardiogenic shock.

It has been reported that abnormalities of atrial conduction are present in patients with atrial flutter (AFL). We analyzed the P wave signal-averaged ECG (PSE) in patients after cardioversion of chronic AFL by radiofrequency catheter ablation (RFCA) to determine whether abnormalities of atrial conduction exist in patients with AFL and whether they recover. We studied 11 patients undergoing ablation of persistent AFL (AFL group), 11 patients with paroxysmal AFL (PAFL group), and 14 patients without any evidence of arrhythmias (control group). The PSEs were recorded 1 day, 7 days, and 1 month after RFCA. The filtered P wave duration (FPD) was calculated from the PSE recording. The FPD correlated with interatrial conduction time (r = 0.644) and left atrial dimension (r = 0.675) in combined assessment of the AFL and PAFL groups. The FPD was longer in the AFL group 1 day (165 +/- 14 ms, P0.001) and 1 month (150 +/- 18 ms, P0.05) after RFCA than in the control group (134 +/- 10 ms). Our findings suggest that atrial conduction abnormalities detected by PSE are present in patients with persistent AFL and improve 1 month after cardioversion.

Because atherosclerotic plaque burden affects the likelihood of plaque rupture, it is important to determine the presence and extent of atherosclerotic plaque. We hypothesized that endothelial dysfunction becomes more prominent with development of atherosclerotic plaque; therefore, we examined the relation between coronary endothelial dysfunction and the presence of atherosclerotic plaque. In 36 patients with normal coronary arteries, acetylcholine (ACh; 3 and 30 microg/min) and nitroglycerin were infused into the left coronary ostium, and the diameter of the left anterior descending (LAD) coronary artery was quantitatively measured in response to each drug. The plaque burden was measured in the same segment using intravascular ultrasonography. The plaque burden was 31.2 +/- 2.1% and correlated inversely with changes in coronary diameter induced by 3 microg/min of ACh (r = -0.754, p0.0001), 30 microg/min of ACh (r = -0.552, p = 0.0005), and nitroglycerin (r = -0.531, p = 0.0009). Multivariate regression analysis showed that the change in coronary diameter induced by 3 microg/min of ACh was associated with plaque burden, independent of the effects of nitroglycerin-induced dilation. Receiver-operating characteristics analysis demonstrated that a cut-off value for the change in coronary diameter induced by 3 microg/min of ACh for predicting a plaque burden of30% was 0%, with a sensitivity of 0.82 and a specificity of 0.95. These findings suggest that coronary endothelial dysfunction is correlated with atherosclerotic plaque burden, indicating that atherosclerotic plaque may be detected based on coronary endothelial function as assessed by low-dose ACh infusion.

Few studies have investigated the long-term angiographic outcome of successful coronary balloon angioplasty (CBA) among diabetic and nondiabetic dilated lesions. The purpose of this study was to evaluate and compare the long-term (>5 years) outcomes of diabetic and nondiabetic CBA lesions which had remained patent 3-12 months after intervention. Twenty-five patients (45 lesions) with diabetes mellitus and 79 patients (138 lesions) without diabetes mellitus were enrolled as subjects. All patients who underwent CBA without restenosis within 3-12 months of the initial CBA based on follow-up angiographic evaluation were included. Quantitative coronary angiograms performed before, immediately after CBA, during the 3-12-month period (mean 4.1 +/- 1.0 months), and at or after 5 years (mean 6.4 +/- 2.0 years) were compared. There was no significant difference in the reference diameter between nondiabetic and diabetic lesions at any of the four time points studied. The minimum lumen diameter before and immediately after the procedure and at the 3-12-month follow-up did not differ significantly between the two groups. At >5-year follow-up. the minimum lumen diameter was significantly (P = 0.005) decreased in diabetic lesions. Total occlusion occurred in 9% (4/45) of the diabetic lesions compared to only 1%, (1/138) in the nondiabetic lesions (P = 0.007). Diabetic lesions showed significant (P = 0.049) narrowing between the 3-12 month period and >5-year follow-up. Fifty-one percent (18/35) of the nondiseased vessels in the diabetic patients at the time of enrollment had new stenosis during the follow-up periods. In conclusion, compared to nondiabetic lesions, patients with diabetic lesions who underwent CBA were more predisposed to have stenotic progression and total occlusion.

A 67-year-old female with paroxysmal atrial fibrillation successfully underwent circumferential pulmonary vein isolation (CPVI). Nine months later, a thrombus formation on the previous CPVI line was occasionally observed in the left atrium by follow-up transoesophageal echocardiography. This is a rare case with a late detection of a clot on the previous CPVI line in spite of receiving dabigatran. …

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Association between obesity and hypertension has been well recognized. A reduction in the body weight of over-weight hypertensive patients is a recommended lifestyle modification. The purpose of our study is to examine the relationship of insulin sensitivity and autonomic nervous activity with reduction of blood pressure by the calorie restriction. We evaluated the heart rate variability, nocturnal change of blood pressure and insulin resistance before and after a short-term low-calorie diet in 12 overweight essential hypertensives. After a week of standard diet (2000 kcal), 2 weeks of low-calorie diet (800 kcal) with normal sodium content induced a significant reduction in body mass index, triglyceride, fasting immunoreactive protein, homeostasis model assessment as an index of insulin resistance, and urinary excretion of sodium and potassium. Systolic blood pressure was significantly reduced both in daytime and night-time after the low-calorie diet (daytime, 134.5+/-6.0 to 122.0+/-4.1 mmHg; night-time, 126.8+/-5.2 to 113.4+/-7.2 mmHg). In daytime, diastolic blood pressure was also reduced (90.3+/-2.1 to 88.1+/-4.8 mmHg). Although heart rate was not significantly reduced, a rise of high frequency in night-time (346+/-82 to 572+/-108 ms2) and a fall of low frequency/high frequency in day-time (3.5+/-0.4 to 2.6+/-0.1) was significant after a low-calorie diet. In conclusion, weight loss by low-calorie diet with a constant intake of sodium, reduced blood pressure in obese hypertensives by improvement of vagal nervous activity and insulin resistance.

High on-treatment platelet reactivity (HTPR) has been reportedly associated with adverse ischemic events after coronary intervention. A recent study showed “thrombo-restenosis” pattern in restenotic lesions after coronary stent implantation by using optical coherence tomography. However, an

Restriction fragment length polymorphisms of the vitamin D receptor gene have recently been reported to be associated with changes in bone mineral density. Alterations in systemic calcium balance and Ca-regulating hormones such as 1,25(OH)2 vitamin D3 and parathyroid hormone have been demonstrated in essential hypertension. We investigated the relationship between polymorphisms of the vitamin D receptor gene and systemic Ca metabolism in patients with essential hypertension and in normotensives. We compared 147 subjects with essential hypertension and 100 normotensive control subjects. The genotype distribution and derived allele frequencies for the vitamin D receptor gene were similar in the two groups (genotype bb/Bb/BB and allele B/b: 60.1/32.6/7.2 and 0.24/0.76 in hypertensives vs. 56.0/36.0/8.0 and 0.26/0.74 in normotensive subjects). Serum concentrations of total Ca in the bb, Bb, and BB groups were, respectively, 4.5+/-0.3 vs. 4.5+/-0.4 vs. 4.4+/-0.5 mmol/l in normotensives and 4.6+/-0.3 vs. 4.6+/-0.4 vs. 4.4+/-0.5 mmol/l in hypertensives. Ionized Ca levels were 1.17+/-0.04 vs. 1.16+/-0.04 vs. 1.15+/-0.04 mmol/l in normotensives and 1.16+/-0.04 vs. 1.16+/-0.04 vs. 1.14+/-0.05 mmol/l in hypertensives, respectively. These results indicate that the BB genotype of the vitamin D receptor gene is associated with lower serum Ca levels but is not a useful predictive marker for the development of essential hypertension in Japanese subjects.

Object. In hypercholesterolemic patients, acetylcholine- and substance P-mediated endothelium-dependent dilation of the coronary resistance vessels is impaired due to decreased nitric oxide production. However, it is not clear if bradykinin-induced coronary vasodilation is impaired in these patients. We investigated whether the endothelium-dependent dilation of coronary resistance vessels mediated by bradykinin is impaired in patients with hypercholesterolemia and, if so, whether this impairment is caused by a decreased production of nitric oxide. Methods. We examined the coronary vascular responses to acetylcholine and bradykinin. The vascular responses to bradykinin were also assessed after NG-monomethyl-L-arginine was infused to inhibit nitric oxide production. Drugs were infused into the left coronary ostium and coronary blood flow (CBF) and coronary vascular resistance were evaluated by quantitative angiography and Doppler flow velocity measurements. Patients. Twelve hypercholesterolemic patients and 11 control patients with angiographically normal coronary arteries were studied. Results. The vasodilator responses to acetylcholine and bradykinin were reduced in hypercholesterolemic patients compared with control patients (p

Idiopathic ventricular tachycardias (VTs) are generally divided into those arising from the right ventricle and those arising from the left ventricle. There has been few reports of two morphologically distinct VT occurring in patients with no apparent structural heart disease. We report a patient with verapamil-sensitive left VT with a right bundle branch block pattern that spontaneously changed to VT with a left bundle branch block pattern. Ventricular fibrillation was induced by the application of programmed stimulation. Although it is unclear if our patient with pleomorphic VT has ventricular vulnerability, it is necessary to investigate further and follow him carefully.

Object: This study was performed to compare the coronary microvascular response to adenosine 5'-triphosphate (ATP) with the response to adenosine in humans. Methods: Coronary blood flow velocity was determined using a Doppler flow wire. After intracoronary nitroglycerin infusion, intracoronary bolus injections of adenosine (20 μg) and ATP (20 μg) were performed to induce reactive hyperemia. Patients: Twenty-nine patients (23 men and 6 women, mean age: 63±9 years) with coronary artery disease and risk factors for coronary atherosclerosis were studied. Results: Coronary flow reserve in response to ATP was similar to that for adenosine (2.7±0.7 vs. 2.7±0.7). However, the duration of ATP-induced vasodilation was longer than that of adenosine-induced dilation (39±25 seconds vs. 26±12 seconds, p

We compared bridging and nonbridging coronary artery segments with respect to the vasoconstrictor effect of acetylcholine. Bridging segments were hypersensitive to the constrictor effect of acetylcholine, and results suggest that the effect of nitric oxide on the acetylcholine-stimulated condition is decreased, or that the smooth muscle sensitivity to acetylcholine is increased.

Objectives.This study was performed to evaluate the frequency dependency of ventricular repolarization and the effect of epinephrine in patients with congenital long QT syndrome (LQTS).Background.The efficacy of pacemakers in addition to antiadrenergic therapy in the treatment of congenital LQTS has been reported.Methods.Monophasic action potentials were recorded from right and left ventricular endocardium during atrial pacing at heart rates from 70 to 140 beats/min at baseline and from 100 to 140 beats/min during epinephrine infusion (0.1 μg/kg body weight per min) in 11 patients with congenital LQTS and 10 control patients. The response of monophasic action potential duration at 90% repolarization (MAPD90) and the dispersion of MAPD90 were examined.Results.At baseline, both the MAPD90 and the dispersion of MAPD90 were significantly (p < 0.001) longer in the congenital LQTS group than the control group. The differences in these variables between the two groups significantly decreased (MAPD90: from 105 to 31 ms; dispersion of MAPD90: from 55 to 13 ms, p < 0.001) as heart rate was increased. Epinephrine prolonged the MAPD90 and increased the dispersion of MAPD90 significantly (p < 0.001) at all paced heart rates in the congenital LQTS group without frequency dependency but did not change in the control group. Thus, epinephrine increased the differences in these variables between the two groups.Conclusions.The repolarization abnormalities in congenital LQTS were attenuated by increasing the heart rate, which supported the efficacy of pacemaker therapy. However, during sympathetic stimulation, the effects of increased heart rate on these repolarization abnormalities were limited.

Several clinical studies have shown that patients with congenital long QT syndrome (LQTS) have primary ventricular repolarization abnormalities, which are characterized by prolongation and increased dispersion of ventricular repolarization. Recently, efficacy of pacemakers has been reported as a therapy for LQTS patients in addition to β -adrenergic blocking drugs. The present study was performed to evaluate the influence of different heart rate on ventricular repolarization in LQTS patients. We recorded monophasic action potentials (MAPs) with a contact electrode during right atrial pacing. MAPs were obtained simultaneously from two to four sites at the right and left ventricular endocardium in 9 LQTS patients (28 sites) and 7 control patients (17 sites). Heart rate was changed from 70/min to 140/min by using right atrial pacing, then MAP duration at 90% repolarization (MAPD90) and dispersion of MAPD90 (difference between the longest MAPD90 and the shortest MAPD90 in each patients) in relation to heart rate were examined at steady state. Results 70/min 80/min 100/min 120/min 140/min MAPD90(ms) (LQTS; n = 28) 392 ± 58 *** 347 ± 56 *** 316 ± 44 *** 284 ± 31 *** 239 ± 17 ** (Control; n = 17) 303 ± 16 275 ± 22 249 ± 24 234 ± 19 199 ± 10 Δ 89 72 67 50 40 70/min 80/min 100/min 120/min 140/min Dispersion of MAPD90 (ms) (LQTS; n = 9) 79 ± 18 ** 59 ± 20 * 39 ± 19 34 ± 17 25 ± 21 (Control; n = 7) 27 ± 6 28 ± 8 21 ± 7 21 ± 7 15 ± 14 Δ 52 31 18 13 10 Δ; difference between mean value in LQTS patients and that in control patients at each heart rate * P l 0.05 ** P l 0.005 *** P l 0.0005 v.s. control patients Conclusion Repolarization abnormalities were attenuated gradually by increasing heart rate in LQTS patients, which supported the efficacy of pacemaker therapy in this syndrome.