Jeong Cheon Ahn

Spatial Dispersion of Action Potential Duration Restitution Kinetics Is Associated with Induction of Ventricular Tachycardia/Fibrillation in Humans

Introduction: Action potential duration restitution (APDR) plays a role in initiation and maintenance of ventricular tachycardia (VT)/ventricular fibrillation (VF). We hypothesized that the steeply sloped APDR and its spatial heterogeneity contribute to VT/VF inducibility in patients with ventricular arrhythmia.

Impact of obstructive sleep apnea on left ventricular diastolic function.

The aim of this study was to investigate the impact of obstructive sleep apnea (OSA) on left ventricular (LV) functional changes by using tissue Doppler imaging-derived indexes in patients with OSA. We studied 62 patients classified into 3 groups, namely 18 with mild to moderate OSA, 24 with severe OSA, and 20 control subjects without OSA according to the apnea-hypopnea index (AHI) on complete overnight polysomnogram. All underwent conventional and tissue Doppler echocardiographies. Only early diastolic velocity (Ea; -6.2 +/- 0.3 vs -7.1 +/- 0.3 vs -7.3 +/- 0.3 cm/s, respectively, for the 3 groups, p = 0.023) was significantly decreased in the severe OSA group. Other echocardiographic parameters of diastolic function such as isovolumic relaxation time, deceleration time, mitral inflow early/late wave velocity ratio, and pulmonary vein systolic/diastolic pulmonary vein velocity ratio were comparable among the 3 groups. AHI was correlated only with tissue Doppler imaging-derived indexes of LV diastolic function (Ea r = -0.382, p = 0.002; Ea/late diastolic velocity r = -0.329, p = 0.009), but not with conventional Doppler indexes. AHI remained a significant predictor of Ea after adjusting for age, heart rate, fasting glucose level, blood pressure, body mass index, and LV mass index in a multiple stepwise linear regression model (p = 0.007). In conclusion, only patients with severe OSA showed a greater impairment of LV diastolic function. Of all echocardiographic parameters of diastolic dysfunction investigated, only Ea was identified as the best index to demonstrate an association between LV diastolic dysfunction and severity of OSA independently of body mass index, diabetes mellitus, and hypertension.

Aortic pulse wave velocity as an independent marker of coronary artery disease.

Background: Arterial stiffness has been known as a major contributory factor to cardiovascular (CV) morbidity and mortality in patients with hypertension. Pulse wave velocity (PWV), a surrogate measurement of large artery damage, has not been ascertained as an independent risk factor of coronary artery disease (CAD). The aim of this study was to assess whether PWV is associated with CV risk. Methods and results: We prospectively enrolled 326 consecutive patients undergoing coronary angiography for the assessment of suspected CAD. Arterial stiffness was assessed through aorto‐femoral PWV using fluid‐filled system. PWV was higher in patients with CAD than those without CAD (12.5 ± 5.1 vs 10.2 ± 3.1 m/s, p < 0.001). In multivariate logistic regression analysis, after entering for age, diabetes and other CV risk factors, PWV remained the significant independent variable for CAD (p = 0.050). When the severity of CAD was expressed as one‐, two‐ or three‐vessel disease, PWV was a significantly associated with the severity of CAD (p < 0.001). Conclusion: Our findings suggest that PWV is an independent risk marker for CAD, as well as strongly associated with the severity of CAD.

Effects of cilostazol on platelet activation in coronary stenting patients who already treated with aspirin and clopidogrel.

Background : A recent study has shown that triple anti-platelet therapy (cilostazol+clopidogrel+aspirin) resulted in a significantly lower restenosis rate after coronary stenting than did conventional therapy (clopidogrel+aspirin). However, the anti-platelet effects of cilostazol, when combined with clopidogrel and aspirin, have not been evaluated. Methods : Low dose cilostazol (50 mg/BID) was given to 47 patients who had already been taking clopidogrel (75 mg/day) and aspirin (100 mg/day) for more than 1 month subsequent to coronary stenting due to AMI and unstable angina. Markers of platelet activation, P-selectin and activated GPIIb/IIIa on platelets, were measured at baseline and 2 weeks after cilostazol treatment. We empirically divided patients into tertiles (low, n=16; moderate, n=14; high group, n=17), according to the baseline P-selectin expression. We then performed a comparative assessment of the anti-platelet effects of cilostazol at baseline and after 2 weeks of cilosatzol administration. Results : P-selectin was significantly decreased after 2 weeks of cilostazol treatment in total patients (n=47, 3.2±2.4% to 2.0±1.9%, p=0.03). This inhibition of P-selectin expression was mainly achieved in the moderate and high P-selectin groups (low group; 1.4±0.5 to 1.9±1.3%, p>0.05, moderate group; 2.5±0.3 to 1.3±0.3%, p<0.05, high group; 5.4±2.7 to 2.7±2.8%, p<0.05). Activated GPIIb/IIIa was not significantly changed (13.5% to 17.6%, p>0.05). Underlying disease, cardiovascular risk factors, concomitant medication including statin, and hsCRP were not related to the degree of P-selectin expression. Conclusion : Our data demonstrated that cilostazol treatment in addition to conventional anti-platelet therapy provides more effective suppression of platelet P-selectin expression in patients with relatively high platelet activity.

Cardioprotective effects of rosuvastatin and carvedilol on delayed cardiotoxicity of doxorubicin in rats

Context: Doxorubicin is widely used anti-neoplastic drug but has serious cardiotoxicity. Long-term cardioprotective effects of statin and carvedilol against delayed cardiotoxicity of doxorubicin was not well elucidated. Objective: To evaluate long-term cardioprotective effects of co-administered rosuvastatin and carvedilol against chronic doxorubicin-induced cardiomyopathy (DIC) in rats. Methods: Sixty-one rats were assigned to six groups: group I, control; group II, doxorubicin only (1.25 mg/kg, bi-daily, I.P.); group III, doxorubicin + rosuvastatin (2 mg/kg/day, P.O.); group IV, doxorubicin + rosuvastatin(10 mg/kg/day, P.O.); group V, doxorubicin + carvedilol (5 mg/kg/day, P.O.); group VI, doxorubicin + carvedilol (10 mg/kg/day, P.O.). Drugs were administered for 4 weeks (by week 4) and rats were observed without drugs for 4 weeks (by week 8). Results: After 4 weeks discontinuation of drugs (week 8), group III showed higher +dP/dt (p = 0.058), lower −dP/dt (p = 0.009), lower left ventricular (LV) tissue malondialdehyde (MDA; p = 0.022), and less LV fibrosis (p = 0.011) than group II. Group IV showed similar results to group III. However, in group V and VI, carvedilol failed to reduce LV dysfunction, elevation of troponin or myocardial fibrosis, although group V showed lower LV tissue MDA (p = 0.004) than group II. Discussion and conclusions: Myocardial injury and LV systolic/diastolic dysfunction at week 8 was alleviated by co-administered rosuvastatin, but not by carvedilol. It is unclear whether the cardioprotective effect of rosuvastatin is attributed to a suppression of oxidative stress induced by doxorubicin, because carvedilol did not exhibit a cardioprotective effect despite its antioxidant effects.

Brugada-Like ST-Segment Abnormalities Associated with Myocardial Involvement of Hematologic Diseases

This is a report of Brugada‐like ST‐segment abnormalities related to acute myocarditis associated with hematologic disorders. Electrocardiographic (ECG) pattern of ST‐segment elevation in the right precordial leads mimicking Brugada syndrome may relate to pathological abnormalities due to hematologic disorders that may have genetic, infective, or inflammatory origins. We describe two cases of myocardial involvement of hemotologic disorders, manifested with Brugada‐like ECG findings.

Papillary fibroelastoma of the pulmonary valve

A papillary fibroelastoma is rare, but it is the most common primary tumor of the cardiac valves. Most papillary fibroelastomas affect the left-sided heart valves, such as the aortic and mitral valves; however, they also rarely affect the pulmonary valve. Generally, surgical removal is strongly recommended to prevent its potential thromboembolic risks, especially in cases of left-sided cardiac involvement. However, there are few reports on the treatment of asymptomatic, small, right-sided cardiac fibroelastomas. We present a rare case of an asymptomatic papillary fibroelastoma occurring on the pulmonary valve, which was detected by transthoracic echocardiography, transesophageal echocardiography, and a 64-slice cardiac computed tomography scan, and which was surgically removed.

Simultaneous and spontaneous multivessel coronary artery dissection presenting as congestive heart failure

Spontaneous coronary artery dissection (SCAD) is a rare cause of myocardial ischemia. Multivessel SCAD is much rarer than single vessel involvement and acute coronary syndrome is the most frequent clinical presentation of a patient with SCAD. The patient in this report had SCAD in both the left anterior descending and right coronary arteries at the same time. However, the clinical manifestation was not acute coronary syndrome but rather congestive heart failure. Successful angioplasty and stent placement was performed and the symptoms of congestive heart failure were successfully resolved with medical treatment.

Inferior vena cava collapsibility index, renal dysfunction, and adverse outcomes in patients with broad spectrum cardiovascular disease

The clinical implication of the inferior vena cava collapsibility index (IVCCI) has not been well evaluated in patients with various cardiovascular diseases.

Primary cardiac lymphoma presenting as an atypical type of hypertrophic cardiomyopathy.

Primary cardiac lymphoma (PCL) is a very rare malignancy although cardiac involvement with the disseminated disease is not uncommon. We present a case of a 43‐year‐old man with PCL that initially presented as marked thickening of all cardiac walls and was mistakenly diagnosed as an atypical type of hypertrophic cardiomyopathy. The diagnosis of PCL was made with a delay of 9 months after the initial presentation, when atypical lymphocytes staining positive for CD79a and CD20 were demonstrated in the rapidly growing mediastinal and neck mass. Anthracycline‐based chemotherapy and anti‐CD20 immunotherapy resulted in a remarkable reduction in cardiac wall thickness and mediastinal mass. The first lesson to be learnt from this case is that PCL can present as a diffuse infiltrative disease without a mass. The second lesson is that prompt exploratory thoracotomy should not be delayed when the diagnosis is elusive.