Search

Background The role of J-waves in the pathogenesis of ventricular fibrillation (VF) occurring in structurally normal hearts is important. Methods We evaluated 127 patients who received an implantable cardioverter-defibrillator (ICD) for Brugada syndrome (BS, n = 53), early repolarization syndrome (ERS, n = 24), and patients with unknown or deferred diagnosis (n = 50). Electrocardiography (ECG), clinical characteristics, and ICD data were analyzed. Results J-waves were found in 27/50 patients with VF of unknown/deferred diagnosis. The J-waves were reminiscent of those seen in BS or ERS, and this subgroup of patients was termed variants of ERS and BS (VEB). In 12 VEB patients, the J/ST/T-wave morphology was coved, although amplitudes were

Objective Hypothermia can induce ECG J waves. Recent studies suggest that J waves may be associated with ventricular fibrillation (VF) in patients with structurally normal hearts. However, little is known about the ECG features, clinical significance or arrhythmogenic potentials of therapeutic hypothermia (TH)-induced J waves. Methods We analysed ECGs from 240 patients who underwent TH at six major university hospitals in Korea between August 2010 and December 2013. The prevalence, amplitudes and distributions of the J waves and the development of malignant arrhythmia were analysed. Results The average patient body temperature was 33.5±1.0°C during TH. J waves were observed in 98 patients (40.8%). They were newly developed in 91 cases, and pre-existing J waves were augmented in seven patients. J waves during TH were primarily observed in leads II, III, aVF and V 4–6 . The average amplitude of the J waves was 0.239±0.152 mV. There were four VF events during TH. These events occurred in three patients who were finally diagnosed with Brugada syndrome, idiopathic VF or early repolarisation syndrome, respectively, and in one patient with non-cardiac aetiology (asphyxia). Conclusions J waves were recorded in about 40% of the patients who received TH. They were most frequently observed in the inferior limb leads or lateral precordial leads. Life-threatening VF occurred only rarely (1.7%) during TH and were mainly observed in patients with primary arrhythmic disorder. Although a causal relationship between TH-induced J waves and VF remains unknown, administering TH to this potentially susceptible, high-risk population may require careful attention.

BACKGROUND AND OBJECTIVES Wall shear stress contributes to atherosclerosis progression and plaque rupture. There are limited studies for statin as a major contributing factor on whole blood viscosity (WBV) in patients with acute coronary syndrome (ACS). This study investigates the effect of statin on WBV in ACS patients. SUBJECTS AND METHODS We prospectively enrolled 189 consecutive patients (mean age, 61.3±10.9 years; 132 males; ST-segment elevation myocardial infarction, n=52; non-ST-segment elevation myocardial infarction, n=84; unstable angina n=53). Patients were divided into two groups (group I: previous use of statins for at least 3 months, n=51; group II: statin-naive patients, n=138). Blood viscosities at shear rates of 1 s-1 (diastolic blood viscosity; DBV) and 300 s-1 (systolic blood viscosity; SBV) were measured at baseline and one month after statin treatment. Rosuvastatin was administered to patients after enrollment (mean daily dose, 16.2±4.9 mg). RESULTS Baseline WBV was significantly higher in group II ([SBV: group I vs group II, 40.8±5.9 mP vs. 44.2±7.4 mP, p=0.003], [DBV: 262.2±67.8 mP vs. 296.9±76.0 mP, p=0.002]). WBV in group II was significantly lower one month after statin treatment ([SBV: 42.0±4.7 mP, p=0.012, DBV: 281.4±52.6 mP, p=0.044]). However, low-density lipoprotein cholesterol level was not associated with WBV in both baseline (SBV: R2=0.074, p=0.326; DBV: R2=0.073, p=0.337) and after one month follow up (SBV: R2=0.104, p=0.265; DBV: R2=0.112, p=0.232). CONCLUSION Previous statin medication is an important determinant in lowering WBV in patients with ACS. However, one month of rosuvastatin decreased WBV in statin-naive ACS patients.

Atrial fibrillation (Afib) is the most common arrhythmia with clinical significance, and its incidence increases with advanced age. Afib is associated with a 3- to 5-fold increased risk of stroke, a 3-fold increase in the risk of heart failure, and higher mortality than without Afib. The treatment of Afib is multifold but revolves around one essential issue: whether to attempt to restore sinus rhythm or to simply control the ventricular rate. This decision depends on symptom severity, the age of the patient, underlying heart disease, and other comorbidities that may limit therapeutic options. The management of Afib with antiarrhythmic medications was reviewed. (Korean J Med 2016;90:198-205)

Background/aims Pheochromocytoma and paraganglioma (PPGL) are catecholamine-producing tumors that can cause blood pressure (BP) elevation and cardiovascular complications. Clinical presentation of these tumors may be changed through widespread use of imaging studies, which enables detection of PPGLs before onset of symptoms. We investigated clinical profiles of patients with surgically resected PPGLs. Methods From 2005 to 2017, 111 consecutive patients with surgically resected PPGLs in two tertiary hospitals in Korea were studied. Results Mean age was 52 ± 16 years, 57 patients (51.4%) were male and 54 (48.6%) were hypertensive. Twenty-nine PPGLs (26.1%) were extra-adrenal paragangliomas. Sixteen (14.4%) and seven patients (6.3%) (Group 1, n = 23) were diagnosed during work-up of hypertension and transient cardiomyopathy respectively, and the remainder (Group 2, n = 88) were incidentalomas detected during routine abdominal imaging. Patients in the Group 1 were younger and more frequently symptomatic, and had higher BPs, heart rates and levels of urinary catecholamines than those in the Group 2. Paragangliomas were less frequent and secretion of epinephrine and metanephrine was more predominant in the Group 1 than in Group 2. After the surgical resections, 18.2% of patients still needed antihypertensive medications. Conclusion Out of 111 patients with surgically resected PPGLs, 88 (79.3%) were diagnosed as incidentalomas. Seven patients presented with transient cardiomyopathy and 16 with hypertension. Tumor location and secretion of catecholamine may vary depending on the presence of symptoms.

Background and Objectives Recent studies showed that, in addition to parasympathetic nerves, cervical vagal nerves contained significant sympathetic nerves. We hypothesized that cervical vagal nerve stimulation (VNS) may capture the sympathetic nerves within the vagal nerve and activate the stellate ganglion. Materials and Methods We recorded left stellate ganglion nerve activity (SGNA), left thoracic vagal nerve activity (VNA), and subcutaneous electrocardiogram in seven dogs during left cervical VNS with 30 seconds on-time and 30 seconds off time. We then compared the SGNA between VNS on and off times. Results Cervical VNS at moderate (0.75 mA) output induced large SGNA, elevated heart rate (HR), and reduced HR variability, suggesting sympathetic activation. Further increase of the VNS output to >1.5 mA increased SGNA but did not significantly increase the HR, suggesting simultaneous sympathetic and parasympathetic activation. The differences of integrated SGNA and integrated VNA between VNS on and off times (ΔSGNA) increased progressively from 5.2 mV-s {95% confidence interval (CI): 1.25-9.06, p=0.018, n=7} at 1.0 mA to 13.7 mV-s (CI: 5.97-21.43, p=0.005, n=7) at 1.5 mA. The difference in HR (ΔHR, bpm) between on and off times was 5.8 bpm (CI: 0.28-11.29, p=0.042, n=7) at 1.0 mA and 5.3 bpm (CI 1.92 to 12.61, p=0.122, n=7) at 1.5 mA. Conclusion Intermittent cervical VNS may selectively capture the sympathetic components of the vagal nerve and excite the stellate ganglion at moderate output. Increasing the output may result in simultaneously sympathetic and parasympathetic capture.

To investigate the relationship between heart rate and temperature, we examined 493 febrile patients with documented disease. These patients were diagnosed serologically and analyzed retrospectively: 337 (68.4%) responded to fever with increased heart rate < 10 beats/minute/°C (relative bradycardia [RB]), and 156 patients had a heart rate response ≥ 10 beats/minute/°C (general heart rate increase [GHRI]). The RB group had a higher median resting heart rate and lower heart rate at maximum temperature than the GHRI group. Despite differences in heart rate response, no significant differences were seen in clinical outcomes (acute kidney injury, systemic inflammatory response syndrome (SIRS), and death). We concluded that most patients with scrub typhus presented with RB. In scrub typhus infection, RB can be included as one of the clinical features for differential diagnosis from other infectious diseases.

Introduction We tested the hypothesis that subcutaneous nerve activity (SCNA) of the thorax correlates with the stellate ganglion nerve activity (SGNA) and can be used to estimate the sympathetic tone.

The relationship between cardiac autonomic nerve activity and blood pressure (BP) changes in ambulatory dogs is unclear.The purpose of this study was to test the hypotheses that simultaneous termination of stellate ganglion nerve activity (SGNA) and vagal nerve activity (VNA) predisposes to spontaneous orthostatic hypotension and that specific β₂-adrenoceptor blockade prevents the hypotensive episodes.We used a radiotransmitter to record SGNA, VNA, and BP in eight ambulatory dogs. Video imaging was used to document postural changes.Of these eight dogs, five showed simultaneous sympathovagal discharges in which the minute-by-minute integrated SGNA correlated with integrated VNA in a linear pattern (group 1). In these dogs, abrupt termination of simultaneous SGNA-VNA at the time of postural changes (as documented by video imaging) was followed by abrupt (20 mm Hg over four beats) drops in BP. Dogs without simultaneous on/off firing (group 2) did not have drastic drops in pressure. ICI-118,551 (ICI, a specific β₂-blocker) infused at 3 µg/kg/h for 7 days significantly increased BP from 126 mm Hg (95% confidence interval 118-133) to 133 mm Hg (95% confidence interval 125-141; P = .0001). The duration of hypotension (mean systolic BP100 mm Hg) during baseline accounted for 7.1% of the recording. The percentage was reduced by ICI to 1.3% (P = .01).Abrupt simultaneous termination of SGNA-VNA was observed at the time of orthostatic hypotension in ambulatory dogs. Selective β₂-adrenoceptor blockade increased BP and reduced the duration of hypotension in this model.

Background and objectives Acute myocardial infarction-related heart failure (HF) is associated with poor outcome. This study was designed to investigate the usefulness of global longitudinal strain (GLS), global circumferential strain (GCS) and mean longitudinal strain of left anterior descending artery territory (LSant) measured by 2-dimensional speckle tracking echocardiography (2D STE) in prediction of acute anterior wall ST-segment elevation myocardial infarction (ant-STEMI)-related HF. Methods A total of 171 patients with ant-STEMI who underwent successful primary coronary intervention and had available 2D STE data were enrolled. Patients were divided into 3 groups: in-hospital HF, post-discharge HF, and no-HF groups. Results In-hospital and post-discharge HF developed in 39 (22.8%) and 13 (7.6%) of patients, respectively and 113 patients (69.6%) remained without HF. Multivariate analysis showed that GLS was the only factor significantly associated with the development of in-hospital HF. For post-discharge HF, LSant was the only independent predictor. Other echocardiographic or laboratory parameters did not show independent association with the development of ant-STEMI-related HF. Conclusions GLS is a powerful echocardiographic parameter related to development of in-hospital HF and LSant was significantly associated with post-discharge HF in patients with successfully reperfused ant-STEMI.

Small conductance calcium activated potassium (SK) currents are abundantly present in the neurons1, 2 and in atrial cardiomyocytes.3–6 However, little or no apamin-sensitive K currents are present in normal ventricles.3, 7, 8 These channels are activated by increases in intracellular Ca2+ (Cai) and are blocked by apamin.2 In the nervous system, activation of apamin-sensitive K+ current (IKAS) is responsible for slow afterhyperpolarizations, which help terminate neuronal action potential bursts.9 Similar to rapid neuronal discharges, ventricular fibrillation (VF) also causes Cai accumulation that may persist minutes after successful defibrillation.10 Cai accumulation and acute postshock action potential duration (APD) shortening facilitated the development of late phase 3 early afterdepolarization (EAD)11 (also known as Cai transient triggered firing)12, 13 and electrical storm in that model. The acute postshock APD shortening in failing ventricles was shown to be due to IKAS activation.8 A more recent study by Chang et al14 showed that both the IKAS and the SK protein are increased in the native hearts of transplant recipients, and that apamin significantly prolongs the APD in failing human ventricular myocytes but not in normal control ventricular myocytes. These findings suggest that IKAS is important in ventricular repolarization and arrhythmogenesis in failing ventricles by shortening APD during Cai accumulation. However, the ability to accelerate the repolarization may also be antiarrhythmic. The redundancy in the complexities of myocardial repolarization (repolarization reserve)15 is important in maintaining normal and orderly ventricular repolarization, while reduced repolarization reserve underlies the mechanisms of afterdepolarization and ventricular arrhythmias in congenital or acquired long-QT syndromes.16 Myocardial infarction (MI) is followed by significant arrhythmogenic ion-channel remodeling including downregulation of multiple K currents in the peri-infarct zone as well as in the subendocardial Purkinje fibers.17 These changes were thought to underlie the mechanisms of afterdepolarizations and ventricular arrhythmias in MI ventricles. While K current remodeling after MI has been extensively studied, none of these studies included an evaluation of IKAS after MI. If there is an increased IKAS, it would counterbalance the downregulation of other K currents, hence maintaining repolarization reserve. Inhibition of IKAS by apamin would prolong the APD and reduce the repolarization reserve. The purpose of the present study was to perform optical mapping studies and patch clamp studies to test the hypothesis that IKAS is increased in rabbit ventricles with chronic MI and contributes significantly to ventricular repolarization in MI ventricles.

Objectives As most clinical studies measure whole blood viscosity (WBV) from peripheral samples, potential differences in WBV obtained from the coronary arteries are often ignored. This study investigated differences in WBV measured from coronary artery specimens in patients with and without acute coronary syndrome (ACS). Methods and results Consecutive patients with chest pain who underwent diagnostic coronary angiography were divided into two groups [non-ACS (n = 16), ACS (n = 22)]. The ACS group consisted of unstable angina (n = 13) and acute myocardial infarction (n = 9) patients. Two blood samples were obtained from each patient at the both coronary artery ostia prior to coronary angiography. Low-shear and high-shear blood viscosities (BVs) were measured at shear rates of 1 and 300 s-1, respectively, by a scanning capillary tube viscometer (Bio-Visco Inc., South Korea). Both low-shear and high-shear BVs obtained from peripheral, left and right coronary arteries were not different in both groups. Mean coronary low-shear WBV values obtained in ACS group were 29.2% higher than those in non-ACS group (295.3 ± 87.2 mP vs. 228.5 ± 69.2 mP, p = 0.016). Mean coronary high-shear WBV values obtained in ACS group were 15.6% higher than those in non-ACS group (42.9 ± 10.0 mP vs. 37.1 ± 4.6 mP, p = 0.036). Conclusions Direct measurement of WBV from the coronary artery showed no differences with peripheral samples. Future larger studies are needed to clarify our results.

The role of J-waves in the pathogenesis of ventricular fibrillation (VF) occurring in structurally normal hearts is important.We evaluated 127 patients who received an implantable cardioverter-defibrillator (ICD) for Brugada syndrome (BS, n = 53), early repolarization syndrome (ERS, n = 24), and patients with unknown or deferred diagnosis (n = 50). Electrocardiography (ECG), clinical characteristics, and ICD data were analyzed.J-waves were found in 27/50 patients with VF of unknown/deferred diagnosis. The J-waves were reminiscent of those seen in BS or ERS, and this subgroup of patients was termed variants of ERS and BS (VEB). In 12 VEB patients, the J/ST/T-wave morphology was coved, although amplitudes were0.2 mV. In 15 patients, noncoved-type J/ST/T-waves were present in the right precordial leads. In the remaining 23 patients, no J-waves were identified. VEB patients exhibited clinical characteristics similar to those of BS and ERS patients. Phenotypic transition and overlap were observed among patients with BS, ERS, and VEB. Twelve patients with BS had background inferolateral ER, while five ERS patients showed prominent right precordial J-waves. Patients with this transient phenotype overlap showed a significantly lower shock-free survival than the rest of the study patients.VEB patients demonstrate ECG phenotype similar to but distinct from those of BS and ERS. The spectral nature of J-wave morphology/distribution and phenotypic transition/overlap suggest a common pathophysiologic background in patients with VEB, BS, and ERS. Prognostic implication of these ECG variations requires further investigation.

In the present study, we investigated the effect of guggulsterone on melanogenesis in B16 melanoma cells and elucidated its possible mechanism of action. The effects of guggulsterone on melanogenesis were determined by assaying melanin synthesis and cellular tyrosinase activity in B16/F10 mouse melanoma cells. Guggulsterone dose-dependently inhibited isobutylmethylxanthine (IBMX)-induced melanogenesis and cellular tyrosinase activity with no cytotoxicity. Decreased melanin biosynthesis was accompanied by the reduced expression of melanogenesis-related genes, such as tyrosinase, microphthalmia-associated transcription factor, tyrosinase-related protein (TRP)-1 and TRP-2. Guggulsterone also inhibited α-melanocyte stimulating hormone- or forskolin-induced increases in melanogenesis, suggesting an action on the cAMP-dependent melanogenic pathway. Co-incubation with chenodeoxycholic acid, a well-known farnesoid-X receptor agonist, did not affect IBMX-induced melanogenesis. These results suggest that guggulsterone exerts a melanogenic inhibitory effect through the downregulation of tyrosinase expression.

Background: In typical atrioventricular nodal reentrant tachycardia, radiofrequency (RF) ablation of the slow pathway (SP) is known to change the effective refractory period of the fast pathway (ERPFP) after successful RF ablation of the SP. The purpose of this study was to ascertain the mechanism of the ERPFP changes after SP ablation by comparing the results of both cryo- and RF ablation. Methods and Results: A total of 112 patients were enrolled prospectively and their electrophysiological properties analyzed before and after successful SP ablation. Patients were grouped into cryoablation (n=54) and RF ablation (n=58) groups and each group was subdivided into complete ablation (CG) and modification (MG) based on the presence of the SP after successful ablation. CG was performed in 64 patients: 30 by cryoablation and 34 by RF ablation. In patients who underwent complete SP ablation, the ERPFP was shortened significantly after cryoablation (375±74 vs. 281±39ms, P

Background Meta-analysis of randomized trials showed superior efficacy and similar safety of drug-eluting stent over bare-metal stent in acute ST-elevation myocardial infarction (STEMI) patients. However, long-term relative outcomes of sirolimus- (SES) vs. paclitaxel-eluting stent (PES) have not been fully evaluated in randomized studies. This study compared long-term safety and efficacy of these two stents in STEMI. Methods A total of 308 STEMI patients were randomly treated with SES ( n =154) or PES ( n =154). Three-year clinical outcomes were assessed. Primary outcome of interest was incidence of major adverse cardiac events (MACE) including death, myocardial infarction (MI), stent thrombosis or target vessel revascularization (TVR). Secondary outcome of interest was occurrence of very late stent thrombosis. Results Both groups had similar baseline characteristics. During follow-up, there was no difference between the two groups in terms of death (6.5% for SES and 10.4% for PES, p =0.22), MI (2.6% vs. 3.9%, p =0.75), stent thrombosis (1.9% vs. 3.2%, p =0.72), TVR (3.9% vs. 8.4%, p =0.15) and MACE (12.3% vs. 18.8%, p =0.12). Eight patients in overall population had stent thrombosis: definite 3, probable 1, and possible 4. Cumulative incidence of stent thrombosis was gradually increased; 0.6% at 30days, 0.6% at 1year, 1.6% at 2years, and 2.6% at 3years. Very late stent thrombosis, definite or probable, occurred in 0.6% for both. Conclusion Among non-selected STEMI patients who underwent primary angioplasty, both SES and PES might be safe and SES showed similar three-year clinical outcomes compared to PES.

Background and Objectives: The development of contrast-induced nephropathy (CIN) is associated with an increased risk of death and late cardiovascular events after percutaneous coronary intervention (PCI). The relationship between CIN and hemoglobin drop has been controversial. The aim of this study was to evaluate the clinical usefulness of periprocedural hemoglobin drop as a nontraditional risk factor for CIN. Subjects and Methods: Five-hundred thirty-seven patients who underwent PCI were divided into 2 groups: Group I (486 patients: patients who did not develop CIN) and Group II (51 patients: patients who developed CIN). All patients were administered iodixanol as contrast media during coronary angiography. CIN is defined as a rise in serum creatinine of ≥25% or ≥0.5 mg/dL above the baseline value within 48 hours after contrast administration. Results: Baseline clinical and cardiovascular risk factors were not significantly different between the two groups, except for low abdominal circumference (Group I : Group II=87.9±9.0 cm : 81.2±15.1 cm, p=0.024), body weight (Group I : Group II= 63.5±10.6 kg : 59.7±9.2 kg, p=0.008), body mass index (BMI) (Group I : Group II=24.4±3.4 kg/m 2 : 23.4± 2.8 kg/m 2 , p=0.032), pre-PCI hemoglobin (Group I : Group II=13.2±2.0 g/dL : 12.3±2.0 g/dL, p=0.003), and post-PCI hemoglobin (Group I : Group II=12.4±1.9 g/dL : 11.5±1.8 g/dL, p=0.001). Multiple logistic regression analysis showed that a periprocedural drop in hemoglobin (>1 g/dL) was an independent predictor of CIN, like other known risk factors. Conclusion: A periprocedural drop in hemoglobin of more than 1 g/dL is another important independent predictor for CIN, even in patients administered the lowest nephrotoxic contrast agent, iodixanol, during PCI. (Korean Circ J 2010;40:68-73)

Background Atrial tachyarrhythmias (ATA) frequently develop during catheter ablation of atrial fibrillation (AF), but the mechanism of ATA during combined pulmonary vein isolation (PVI) and complex fractionated electrogram-guided ablation (CFEA) has not been reported. Methods and results This study involved 105 patients with symptomatic, drug-refractory AF. After PVI, CFEA was performed in the left/right atrium if AF remained inducible in paroxysmal AF (PAF) or persisted in persistent AF (PeAF). For the 70 PAF patients, PVI alone rendered AF non-inducible in 29 patients (41.4%), and converted inducible AF into inducible atrial flutter (AFl) in 10 patients (14.3%). For the remaining 31 PAF patients, additional CFEA rendered AF non-inducible in 11 patients (15.7%), whereas only AFl was inducible in 11 patients (15.7%). For 35 PeAF patients, PVI and CFEA converted AF into sinus rhythm in 2 (5.7%) and into AFl in 21 (60.0%) patients, while AF persisted in 12 patients (34.3%). The mechanism of ATA was focal (20/114, 17.5%), roof-dependent (20/114, 17.5%), peri-mitral (33/114, 28.9%), cavotricuspid isthmus-dependent (34/114, 29.8%) AFl or unknown (7/114, 6.1%). Successful ablation was achieved in 93/114 (81.6%) tachycardias. Conclusions The major mechanism of ATA during the combined approach of PVI and CFEA is macroreentry around large anatomic obstacles such as the pulmonary vein or the mitral or tricuspid annuli.

Although cilostazol has decreased restenosis and target lesion revascularization (TLR) after drug-eluting stent implantation, it is not known if this effect is durable at 2 years. We analyzed 2 randomized studies (Drug-Eluting stenting followed by Cilostazol treatment reduces LAte REstenosis in patients with DIABETES mellitus and Drug-Eluting Stenting Followed by Cilostazol treatment reduces LAte REstenosis in patients with LONG native coronary lesions trials) in which 900 patients were randomly assigned to triple antiplatelet therapy (aspirin, clopidogrel, and cilostazol; triple group, n = 450) and dual antiplatelet therapy (aspirin and clopidogrel; standard group, n = 450) for 6 months in patients with diabetes or long lesions receiving drug-eluting stents. We evaluated 2-year major adverse cardiac events (MACEs) including death, myocardial infarction (MI), and TLR. Nine-month TLRs and MACEs were significantly decreased in the triple versus standard group. At 2 years, the triple group sowed significantly decreased TLRs (4.2% vs 9.1%, hazard ratio 0.45, 95% confidence interval 0.26 to 0.78, p = 0.004) and MACEs (5.6% vs 10.4%, hazard ratio 0.52, 95% confidence interval 0.32 to 0.84, p = 0.008) compared to the standard group with no differences in death and MI. In subgroup analysis, triple antiplatelet therapy decrease of 2-year TLR was favorable in all subgroups, especially in patients with paclitaxel-eluting stents, diabetes mellitus, small vessels, long lesions, and left anterior descending coronary artery lesions. In conclusion, compared to the standard group, initial benefit in decreases of 9-month TLRs and MACEs in the triple group was sustained at 2 years with no differences in death or MI. Triple antiplatelet therapy decrease of 2-year TLR was favorable in all subgroups, especially in patients with high-risk profiles.

Primary cardiac leiomyosarcoma is an extremely rare disease entity that is associated with very poor prognosis. We describe here a 45-year-old man who had a huge pleomorphic leiomyosarcoma in the right ventricle (RV) that presented with signs of acute pressure and volume overload and impending obstruction of both outflow and inflow tracts of the RV. The tumor was attached to the RV apex and the interventricular septum, and extended into the main pulmonary trunk just above the pulmonary valve as well as into the right atrium through the tricuspid valve. We evaluated the extent of the tumor using various imaging modalities including transthoracic and transesophageal echocardiography, magnetic resonance imaging, computed tomography, and positron emission tomography-computed tomography. Although he underwent urgent debulking surgery to relieve the obstruction, the tumor could not be resected completely because of its extensive local invasion. The tumor has shown aggressive regrowth after surgery despite adjuvant chemotherapy.

LV thrombus (LVT) formation is one of the major complications of acute anterior wall MI (ant-AMI) and increases risk of embolic events. LV spontaneous echo contrast (SEC) on echocardiography is thought to be a warning of LVT formation. We investigate the incidence, predictors and outcome of LVT and

Although wall shear stress (WSS) is determined by the products of blood viscosity (BV), velocity and lumen diameter, there has been few studies for the direct measurement of WSS by imaging modalities. The aim of our study was to investigate the carotid WSS directly by doppler and BV parameters in

Can Chest Roentgenogram Predict the Posture Dependent Changes of Atrai Performance in Patients with a VDD Pacemaker? The VDD pacemaker is useful for sequential pacing with a single lead but carries a risk of sensing failure. This study was designed to evaluate the relationship between the relative position of atrial lead and atrial sensitivity in different postures in patients with VDD pacemakers. Atrial sensitivity determination and chest roentgenography was performed in the supine and standing position 3 months after implantation in 25 patients with VDD pacemakers. Measurements of cardiac longitudinal length (from the top of the aortic arch to the diaphragm) and distances from the floating electrode to the upper margin of the seventh thoracic vertebra (D-T7), to the top of the aortic arch (D-knob), to the lateral wall of right atrium (D-wall), and the D-knob/cardiac longitudinal length (D-Ratio) were performed. Atrial signal amplitude decreased with the standing compared to the supine position in eight patients (group I) and increased or did not change in the other 17 patients (group II). In group I, the change of the D-ratio was greater (0.073 vs 0.035, P < 0.01), and the change of the cardiac longitudinal length with standing position was greater (18.4 ′ 7.3 vs 12.1 ′ 8.8 mm, P < 0.05) than in group II. The change of atrial sensitivity was related to the change of the atrial electrode position with different postures. Decreased atrial-sensed amplitude was observed in patients who had a greater change in the cardiac longitudinal length while standing. Thus, a decrease in atrial sensitivity with standing may be predicted by the positional changes of the cardiac silhouette on roentgenography before the procedure.

This study devised an automatic monophasic action potential (MAP) measurement program, and compared the computer-measured MAP durations with those measured manually by two independent observers in order to facilitate the analysis of MAP data obtained during a clinical electrophysiology study. The results were compared at various cycle lengths and during pharmacologic or physiologic interventions. This program identified the onset, plateau, and baseline accurately using the MAP data. The automatically measured MAP durations at the 90% repolarization level (MAPd) strongly correlated with those measured manually (r=0.99). The MAPd shortened in parallel as the pacing cycle length was progressively shortened from 800 to 600, 400 and 300 ms .

To demonstrate systolic and diastolic asynchrony in patients with left bundle branch block (LBBB), tissue Doppler imaging (TDI) of 4 different walls was performed in 27 normal controls, 29 patients with right ventricular pacing and normal left ventricular (LV) ejection fraction (EF; pacing LBBB), and 35 patients with idiopathic LBBB. Patients with idiopathic LBBB were further classified into those with LVEF >50% and those with LVEF

Patient initials or identifier number LOR, 1267524 ### Relevant clinical history and physical exam A 74-year-old woman presented to the emergency room with chest discomfort and shortness of breath. She had no history of chronic medical illness. On admission, her blood pressure was 140/90

The objective of this study was to investigate the clinical features of Korean patients with Brugada syndrome (BS). Between June 1998 and April 2002, 15 consecutive patients with BS (13 men, 2 women; mean age, 44+/-10 years) were identified. Eight patients had experienced at least 1 episode of aborted sudden death, 5 patients had had an episode of syncope or chest pain, and 2 patients were asymptomatic at diagnosis. The electrocardiographics (ECGs) of all patients showed spontaneous ST-segment elevation in leads V(1-3) at baseline and 13 patients (87%) showed transient normalization of the ST-segment elevation during follow-up. Twelve patients received an implantable cardioverter-defibrillator (6 patients with aborted sudden death, 5 patients with syncope or chest pain, 1 asymptomatic patient). During a mean follow-up of 19+/-14 months, arrhythmic events occurred in 5 of the 6 patients with aborted sudden death and in 1 of the 5 patients with syncope or chest pain. None of the asymptomatic patients developed any symptoms suggestive of an arrhythmic event. The clinical and ECG manifestation of BS in Korean patients is diverse, but the dynamic nature of the ST segment provides an important clue to the diagnosis of BS. Recurrence of malignant arrhythmia is extremely high in those patients who initially present with aborted sudden death.

KCB-328 [1-(2-amino-4-methanesulfonamidophenoxy)-2-[N-(3,4-dimethoxyphenethyl)-N-methylamino]ethane hydrochloride] is a newly synthesized class III antiarrhythmic drug and is known to be highly effective against various types of arrhythmias induced by coronary artery ligation, reperfusion, and programmed electrical stimulation. To understand the potential ionic mechanisms, we examined the effects of KCB-328, which encodes the rapidly activating delayed rectifier K(+) current in cardiac tissues, on human ether-a-go-go-related gene (HERG) channels expressed in Xenopus oocytes. The amplitudes of steady-state currents and tail currents of HERG were decreased by KCB-328 dose dependently. The decrease became more pronounced at more positive potential, suggesting that the block of HERG by KCB-328 is voltage-dependent. IC(50) values at -30, -20, -10, 0, +10, +20, +30, and +40 mV were 7.6 +/- 0.5, 4.8 +/- 0.4, 3.2 +/- 0.3, 2.1 +/- 0.3, 1.7 +/- 0.2, 1.4 +/- 0.2, 1.3 +/- 0.1, and 1.2 +/- 0.1 microM, respectively. Induction of block depended on depolarization beyond the threshold for channel opening. In addition, time-dependent block developed slowly, with tau = 1.7 +/- 0.3 s (100 microM) at 0 mV, and was delayed by a stronger depolarization to +80 mV, at which HERG channel is inactivated. We can conclude that KCB-328 preferentially blocks open (or activated) HERG channels. The block of HERG current might in part explain the underlying ionic mechanism for the antiarrhythmic and proarrhythmic effect of KCB-328.

Background Predictors of torsades de pointes (TdP) in bradyarrhythmia-induced acquired long QT syndrome are not well defined. Objective The purpose of this study was to search for electrocardiographic (ECG) TdP predictors in patients with acquired atrioventricular block (AVB) and QT prolongation. Methods We analyzed 12-lead ECGs from 20 patients (15 females, age 65.9 ± 15.6 years) with TdP episodes from among 898 AVB patients (2.2%) in 3 tertiary hospitals. The ECG repolarization parameters in TdP patients were compared with those of 80 age- and sex-matched control AVB patients with no TdP episodes. Results TdP was initiated by premature ventricular complexes with a long–short sequence of activation. The average cycle length of the long sequence was 1289.9 ± 228.9 ms and was 2.3 ± 0.6 times longer than the cycle length of the short sequence. TdP patients had a significantly longer mean QT interval (716.4 ± 98.9 ms vs 523.2 ± 91.3 ms, P = .001), mean T peak to end interval (334.2 ± 59.1 ms vs 144.0 ± 73.7 ms, P = .001) and a higher T peak to end interval/QT ratio (0.49 ± 0.09 vs 0.27 ± 0.11, P = .001) compared with non-TdP controls. TdP patients showed a higher prevalence of notched T waves in which T 2 was at least 3 mm taller than T 1 (45.0% vs 1.3%, P = .001), triphasic T waves (30.0% vs 1.3%, P = .001), reversed asymmetry (20.0% vs 0%, P = .001), and T-wave alternans (35.0% vs 0%, P = .001). An algorithm combining these morphologic parameters was able to differentiate TdP patients from non-TdP patients with high sensitivity (85.0%) and specificity (97.5%). Conclusion An algorithm combining specific T-wave morphologies was useful for identifying patients with AVB who are at risk for developing TdP.

We evaluated the efficacy of β-radiation therapy (188Re-MAG3) to inhibit intimal hyperplasia (IH) in diffuse in-stent restenosis by intravascular ultrasound (IVUS) analysis in 50 patients. Nine patients who did not agree with radiation therapy, and therefore underwent rotational atherectomy and balloon angioplasty for diffuse in-stent restenosis in the same study period, were selected for control groups. Serial IVUS comparisons were available in 44 of 50 patients with radiation therapy and 7 of 9 control patients. At 6-month follow-up, there was less significant increase of IH area in patients with radiation therapy than in control patients (Δ IH area = 0.1 ± 0.8 mm2 vs. 2.6 ± 1.8 mm2, P > 0.001 in mean values, and 0.6 ± 1.4 mm2 vs. 2.9 ± 2.1 mm2, P = 0.026 in values of follow-up lesion site, respectively). In conclusion, β-radiation therapy might be an effective treatment modality to inhibit intimal hyperplasia in patients with diffuse in-stent restenosis. Cathet Cardiovasc Intervent 2001;54:169–173. © 2001 Wiley-Liss, Inc.

Background: Atrial mechanical dysfunction and its recovery time course after successful radiofrequency ablation of chronic atrial flutter (AFL) has been largely unknown. We serially evaluated left atrial function by echocardiography after successful ablation of chronic atrial flutter. Methods: In 13 patients with chronic AFL, mitral E wave A wave, and the ratio of A/E velocity were measured at 1 day, 1 month, 3 months and 6–12 months after successful radiofrequency (RF) ablation. Doppler tissue imaging (DTI) technique was also used to avoid load-dependent variation in the flow velocity pattern. Results: Left atrial mechanical function, assessed by A wave velocity and the annular motion, was depressed at 1 day, but improved significantly at 1 month and maintained through 6–12 months after the ablation. Left atrial size did not change significantly. Conclusion: Left atrial mechanical function was depressed immediately after successful RF ablation of chronic AFL, but it improved significantly after 1 month and was maintained over one year.

The aim of this study was to evaluate determinants of coronary blood flow following primary angioplasty (PA) in acute myocardial infarction (AMI). The corrected TIMI (thrombolysis in myocardial infarction) frame count and the TIMI flow grade were used as indexes of coronary blood flow, and its determinants were examined in 115 consecutive AMI patients who underwent PA (pain onset ≤ 12 hr). The following were validated as univariate predictors of slower corrected TIMI frame count: a lower pressure-derived farctional collateral flow (PDCF) index (P < 0.01), poor angiographic collaterals (P < 0.01), TIMI flow 0, 1 before PA (P < 0.05), and the presence of heavy thrombi (P < 0.01). The PDCF index and the presence of heavy thrombi were independent predictors of the corrected TIMI frame count. Likewise, the PDCF index (χ2 = 12.9; P < 0.01) and the presence of heavy thombi (χ2 = 11.4; P < 0.01) were independent predictors of TIMI 3 flow. In conclusion, collateral flow and the presence of thrombi are major determinants of coronary blood flow after PA in AMI. Cathet. Cardiovasc. Intervent. 51:402–406, 2000. © 2000 Wiley-Liss, Inc.

Objective Electrocardiographic markers identifying malignant forms of early repolarisation (ER) from ER of normal variants are of prime clinical importance. We compared the ECG parameters of ER patterns in patients with early repolarisation syndrome (ERS) proximate to the ventricular fibrillation (VF) episodes, remote from the events and those with normal controls with ER. Design A retrospective, case-control study. Setting University hospital. Patients This study included 12 patients with ERS and 36 age-matched, gender-matched controls with ER. Main outcome measures Dynamic change of J-wave. Results The highest amplitude of J-wave, sum of the J-wave amplitudes or the number of leads with ER showed a dramatic change during the perievent period. J-wave amplitudes (2.0±1.3 vs 4.0±1.7, p=0.004) and the number of leads with ER (3.3±1.7 vs 5.3±2.0, p=0.021) were significantly higher around the time of VF. In particular, the characteristic morphology of ‘giant’ (wide, >80 ms) J-waves were observed during the perievent period in 5/12 patients with ERS. However, there were no significant differences in the electrocardiographic parameters of ER pattern remote from VF events between the patients with ERS and normal control subjects with ER. Conclusions Although the extent of and amplitude of J-wave or ST segment elevation (STE) increased significantly around VF episodes, the electrocardiographic parameters of ER remote from VF episodes were not significantly different from those of normal controls. The narrow time window of these ECG changes limits early detection of ER patients at risk of developing VF or sudden cardiac death.

The apamin-sensitive small-conductance calcium-activated potassium current (IKAS ) is increased in heart failure. It is unknown if myocardial infarction (MI) is also associated with an increase of IKAS .We performed Langendorff perfusion and optical mapping in 6 normal hearts and 10 hearts with chronic (5 weeks) MI. An additional 6 normal and 10 MI hearts were used for patch clamp studies. The infarct size was 25% (95% confidence interval, 20-31) and the left ventricular ejection fraction was 50 (46-54). The rabbits did not have symptoms of heart failure. The action potential duration measured to 80% repolarization (APD80 ) in the peri-infarct zone (PZ) was 150 (142-159) milliseconds, significantly (P = 0.01) shorter than that in the normal ventricles (167 [158-177] milliseconds. The intracellular Ca transient duration was also shorter in the PZ (148 [139-157] milliseconds) than that in normal ventricles (168 [157-180] milliseconds; P = 0.017). Apamin prolonged the APD80 in PZ by 9.8 (5.5-14.1)%, which is greater than that in normal ventricles (2.8 [1.3-4.3]%, P = 0.006). Significant shortening of APD80 was observed at the cessation of rapid pacing in MI but not in normal ventricles. Apamin prevented postpacing APD80 shortening. Patch clamp studies showed that IKAS was significantly higher in the PZ cells (2.51 [1.55-3.47] pA/pF, N = 17) than in the normal cells (1.08 [0.36-1.80] pA/pF, N = 15, P = 0.019).We conclude that IKAS is increased in MI ventricles and contributes significantly to ventricular repolarization especially during tachycardia.

Background: The optimal treatment of patients with left main coronary artery (LMCA) dissection during catheter-based procedure remains uncertain. Hypothesis: In cases with significant LMCA dissection occurring during catheter-based procedure, prompt stent implantation may be safe and associated with favorable clinical outcome. Methods: We evaluated the acute and long-term results of bail-out stenting for LMCA dissection occurring during a catheter-based procedure in 10 patients. Results: Initially, there was no significant stenosis of LMCA segments in these patients. Catheter-induced dissection occurred in eight patients (during diagnostic angiography in three patients and during guiding catheter manipulation in five patients). Two patients suffered dissection in the setting of stent deployment in other vessels. Therefore, bail-out stenting for LMCA dissection was performed in a total of 10 patients. In four patients, hypotension developed and an intra-aortic balloon pump was placed during the procedure. Stents were successfully deployed in all patients; there was no in-hospital mortality. Six-month angiographic follow-up was performed in eight patients. No angiographic restenosis (diameter stenosis ≥50%) was observed in any patient at follow-up study. During a mean follow-up of 31 ± 25 months after hospital discharge, there was no major adverse cardiac event (death, myocardial infarction, and target lesion revascularization). Conclusions: Bail-out LMCA stenting is technically feasible and showed good acute and long-term results in a small series of patients.

Background Cervical vagal nerve (CVN) stimulation may improve left ventricular ejection fraction in patients with heart failure. Objectives To test the hypothesis that sympathetic structures are present in the CVN and to describe the location and quantitate these sympathetic components of the CVN. Methods We performed immunohistochemical studies of the CVN from 11 normal dogs and simultaneously recorded stellate ganglion nerve activity, left thoracic vagal nerve activity, and subcutaneous electrocardiogram in 2 additional dogs. Results A total of 28 individual nerve bundles were present in the CVNs of the first 11 dogs, with an average of 1.87±1.06 per dog. All CVNs contain tyrosine hydroxylase-positive (sympathetic) nerves, with a total cross-sectional area of 0.97±0.38 mm 2 . The sympathetic nerves were nonmyelinated, typically located at the periphery of the nerve bundles and occupied 0.03%–2.80% of the CVN cross-sectional area. Cholineacetyltransferase-positive nerve fibers occupied 12.90%–42.86% of the CVN cross-sectional areas. Ten of 11 CVNs showed tyrosine hydroxylase and cholineacetyltransferase colocalization. In 2 dogs with nerve recordings, we documented heart rate acceleration during spontaneous vagal nerve activity in the absence of stellate ganglion nerve activity. Conclusions Sympathetic nerve fibers are invariably present in the CVNs of normal dogs and occupy in average up to 2.8% of the cross-sectional area. Because sympathetic nerve fibers are present in the periphery of the CVNs, they may be susceptible to activation by electrical stimulation. Spontaneous activation of the sympathetic component of the vagal nerve may accelerate the heart rate.

Na channel blockers are effective in suppressing delayed afterdepolarizations (DADs) in isolated Purkinje fibers. However, in isolated mouse ventricular myocytes lacking calsequestrin, only those Na channel blockers that also inhibit type 2 ryanodine receptor channels were effective against spontaneous Ca elevation (SCaE) and DADs.To test the hypothesis that combined Na channel and type 2 ryanodine receptor channel blocker ((R)-propafenone) is more effective than a Na channel blocker (lidocaine) in suppressing SCaE and DADs in the intact rabbit ventricles.We compared (R)-propafenone (3 μmol/L) with lidocaine (50 μmol/L) on SCaE and DADs by using epicardial optical mapping of intracellular calcium (Ca(i)) and membrane voltage in Langendorff-perfused rabbit hearts. SCaE and DADs were induced by rapid pacing trains and isoproterenol (0.3 μmol/L) infusion. One arbitrary unit is equivalent to the Ca transient amplitude of paced beats.SCaEs were observed at the cessation of rapid pacing in all hearts at baseline. (R)-Propafenone nearly completely inhibited DADs and SCaE (0.04 arbitrary units [95% confidence interval 0.02-0.06] vs 0.23 arbitrary units [95% confidence interval 0.18-0.28] at baseline; n = 6 hearts; P.001). Lidocaine also significantly reduced the SCaE but was significantly (P.05) less effective than (R)-propafenone. Both drugs increased the rise time of action potential upstroke and reduced conduction velocity to a similar extent, suggesting a significant inhibition of I(Na).Both Na channel blockers significantly reduced tachycardia-induced SCaEs in the rabbit ventricles, but (R)-propafenone was significantly more effective than lidocaine. These data suggest that type 2 ryanodine receptor inhibition potentiates the activity of Na channel blockers against SCaE and DADs in the intact hearts.

Cardiovascular involvement in Behcet's disease is not uncommon and could be life-threatening. We describe here a 28-year-old man, who developed sudden onset chest pain during warfarinization due to deep vein thrombosis. Echocardiography and computed tomography showed a 60×60 mm-sized hematoma in the pericardial space compressing the right heart. Coronary angiography showed totally occluded proximal right coronary artery. The hematoma was located at the subepicardial plane of the right atrium on surgical view and successfully evacuated. Follow-up echocardiography revealed complete resolution of the hematoma. He is doing well for 24 months after surgery.

Aims The aim of the present study was to identify specific electrocardiogram (ECG) features that predict the development of multiple episodes of ventricular fibrillation (VF) in patients with an early repolarization (ER) pattern and to compare the mode of VF initiation with that observed in typical cases of Brugada syndrome (BrS). Methods and results The mode of the onset and the coupling intervals of the premature ventricular contractions (PVCs) initiating VF episodes were analysed in patients with BrS ( n = 8) or ER who experienced sudden cardiac death/syncope or repeated appropriate implantable cardioverter defibrillator shocks. Among the 11 patients with ER, 5 presented with electrical storm (ES, four or more recurrent VF episodes/day). The five ES patients displayed a dramatic but very transient accentuation of J waves across the precordial and limb leads prior to the development of ES. Ventricular fibrillation episodes were more commonly initiated by PVCs with a short–long–short (SLS) sequence in ER (42/58, 72.4%) vs. BrS patients (13/86, 15.1%, P < 0.01). Coupling intervals were significantly shorter in the ER group compared with those with BrS [328 (320, 340) ms vs. 395 (350, 404) ms, P < 0.01]. Conclusion Our study provides additional evidence in support of the hypothesis that ER pattern in the ECG is not always benign. Transient augmentation of global J waves may be indicative of a highly arrhythmogenic substrate heralding multiple episodes of VF in patients with ER pattern. Ventricular tachycardia/VF initiation is more commonly associated with an SLS sequence, and PVCs display a shorter coupling interval in patients with ER pattern compared with those with BrS.

Even though drug-eluting stent (DES) implantation is an effective treatment for coronary artery stenosis, there are growing concerns related to the real usefulness of DESs due to their increased incidence of thrombosis, stent fracture, and late stent malapposition in comparison to bare metal stents. We have previously reported a case of stent fractures and multiple microaneurysms in both the left anterior descending and left circumflex coronary arteries. In the present case, we demonstrate the ability of dual-source spiral computed tomography to evaluate the various complications of DESs.

Background and Objectives: Local wide split double potentials are used as a parameter to determine complete conduction block during cavotricuspid isthmus ablation in patients with isthmus dependent atrial flutter. However, delayed slow conduction in that region can sometimes be very difficult to differentiate from complete block. Flutter cycle length (FCL) can be used to confirm isthmus conduction block, because FCL is a measure of conduction time around the tricuspid annulus (TA). This study was designed to determine which degree of splitting of the local electrograms is adequate to confirm complete isthmus block, using FCL as a reference. Subjects and Methods: Cavotricuspid isthmus (CTI) ablation was performed in fifty consecutive patients. The interval between the pacing stimulus on the lateral side of the CTI and the first component of the double potentials on the block line (SD1) corresponded to the counterclockwise conduction time. The interval between the pacing stimulus and second component (SD2) represented the clockwise conduction time to the contralateral side of the ablation line. SD1 and SD2 were measured before and after complete isthmus block. Results: An SD1+SD2 reaching 90% of the FCL identified the counterclockwise isthmus conduction block with 94% sensitivity and 100% specificity. Conclusion: If the sum of SD1 and SD2 following isthmus ablation was close to the FCL, complete conduction block was predicted with high diagnostic accuracy and positive predictive value for at least counterclockwise conduction. (Korean Circ J 2009;39:525-531)

Objective: The aim of this study was to compare effectiveness of the Sirolimus- (SES) and Paclitaxel-eluting stent (PES) in primary angioplasty for acute ST-elevation myocardial infarction (STEMI). Background: It has been reported that SES and PES have been more effective than bare-metal stents in reducing restenosis and cardiac events in a broad range of patients with coronary artery disease. However, it is unknown whether there may be differences between these two drug-eluting stents in terms of efficacy in the setting of acute STEMI. Methods: Acute STEMI patients (n = 308) undergoing primary angioplasty were randomly assigned to SES (n = 154) or PES (n = 154) deployment. The routine angiographic follow-up was performed at 6 months and clinical follow-up data was obtained at 12 months. The primary end point was major adverse cardiac events (MACE) including death, reinfarction, stent thrombosis, and target lesion revascularization (TLR) at 12 months. Results: The baseline clinical, angiographic, and procedural characteristics were similar between the 2 groups. Two patients (all from the PES group) experienced stent thrombosis (1 acute and 1 subacute). The SES group revealed lower in-segment restenosis (5.9% vs. 14.8%, P = 0.03) and in-segment late loss (0.09 ± 0.45 vs. 0.33 ± 0.68 mm, P = 0.002) than PES group on follow-up angiography. Twelve-month TLR rates (2.6% vs. 6.5%, P = 0.17) were similar between two groups. MACE rates were lower in the SES group than in the PES group, but it did not reach statistical significance (5.8% vs. 11.7%, P = 0.07). Conclusion: In the setting of primary angioplasty for STEMI, there were no statistically significant differences between the SES and the PES in terms of 12-month MACE. However, binary angiographic in-segment restenosis and in-segment late loss were significantly lower in the SES group. © 2008 Wiley-Liss, Inc.

Sympathetic nervous system and atrial natriuretic peptide (ANP) system play fundamental roles in the regulation of cardiovascular functions. Overactivity of sympathetic nervous system can lead into cardiovascular diseases such as heart failure and hypertension. The present study aimed to define which adrenergic receptors (ARs) affect atrial contractility and ANP release and to determine their modification in renal hypertensive rat atria. An alpha(1)-AR agonist, cirazoline increased ANP release with positive inotropism. These alpha(1)-AR agonist-mediated responses were attenuated by the alpha(1A)-AR antagonist, but not by the alpha(1B)- or alpha(1D)-AR antagonist. An alpha(2)-AR agonist, guanabenz and clonidine increased ANP release with negative inotropism and decreased cAMP level. The order of potency for the increased ANP release was cirazolinephenylephrine=guanabenzclonidine. In contrast, a beta-AR agonist, isoproterenol decreased ANP release with positive inotropism and these responses were blocked by the beta(1)-AR antagonist but not by the beta(2)-AR antagonist. The increased cAMP level by isoproterenol was suppressed by pretreatment with both beta(1)- and beta(2)-AR antagonists. In renal hypertensive rat atria, the effects of isoproterenol on atrial contractility, ANP release, and cAMP level were attenuated whereas the effect of cirazoline on ANP release was unaltered. Atrial beta(1)-AR mRNA level but not alpha(1A)-AR mRNA level was decreased in renal hypertensive rats. These findings suggest that alpha(1A)- and beta(1)-AR oppositely regulate atrial ANP release and that atrial beta(1)-AR expression/function is impaired in renal hypertensive rats.