Characteristics of Cardiac Structural Changes in Patients with Hypertension and Atrial Fibrillation

Backgrounds: Hypertension (HTN) is a major risk factor for the development of atrial fibrillation (AF), and the presence of HTN increases the morbidity and mortality of patients with AF. HTN induces many structural and functional abnormalities of the heart. However, which structural abnormalities are primarily associated with HTN in AF patients still remains to be determined. The aim of this study was to clarify the impact of HTN on the cardiac structural changes in patients with nonvalvular AF (NV-AF). Methods: Two hundred ninety four patients (204males, age: 65.6±11.7years) with NV-AF with a preserved left ventricular (LV) systolic function were included from 6 medical centers. The clinical data was obtained and comprehensive echocardiographic examinations were performed. The patients with HTN (n=169; group 1) were compared with the patients without HTN (group 2). Results: On univariate analysis, the LV mass index (LVMI [105.0±23.0g/m2 vs. 95.7±23.5g/m2]), the left atrial volume index (LAVI [46.4±20.2ml/m2 vs. 40.5±18.9ml/m2]), the deceleration time of the early mitral inflow velocity (DT [163±39ms vs. 175±44ms]), the mitral inflow velocity (E’ [7.7±2.1cm/s vs. 8.3±2.2cm/s]) and the mitral inflow velocity to the diastolic mitral annular velocity (E/E’ [12.1±4.4 vs. 11.0±4.5]) were significanlty different between groups 1 and 2, espectively, (P<0.05 for all). However, on the multivariate analysis, the LV mass index (LVMI), which reflects LV hypertrophy (LVH), was the only factor significantly correlated with HTN in the patients with NV-AF (P<0.05). Conclusion:For patients with NV-AF with a preserved LV function, LVH was a cardiac structural abnormality that was independently associated with co-existing HTN. LVH may be related to the development and maintainence of AF and an increased cardiovascular risk in those patients.ope

Fatal renal bleeding in a patient treated with aggressive antithrombotic therapy after recurrent coronary stent thrombosis

Triple antiplatelet therapy has been known to be superior to the conventional dual regimen for preventing stent thrombosis after coronary stenting, and the addition of oral anticoagulation to antiplatelet therapy is also considered an option. However, the risks and benefits of a triple antiplatelet regimen plus additional oral anticoagulation must be taken into account. Here, we report a case of fatal renal bleeding in a patient treated with triple antiplatelet plus oral anticoagulant therapy for the prevention of recurrent stent thrombosisope

Recovery and recurrence of left ventricular systolic dysfunction in patients with idiopathic dilated cardiomyopathy

BACKGROUND: Some patients with nonischemic left ventricular (LV) systolic failure recover to have normal LV systolic function. However, few studies on the rates of recovery and recurrence have been reported, and no definitive indicators that can predict the recurrence of LV dysfunction in recovered idiopathic dilated cardiomyopathy (IDCMP) patients have been determined. It was hypothesized that patients who recovered from nonischemic LV dysfunction have a substantial risk for recurrent heart failure. METHODS: Forty-two patients (32 men) with IDCMP (mean [+/- SD] age 56.9+/-8.7 years) who recovered from systolic heart failure (LV ejection fraction [LVEF] of 26.5+/-6.9% at initial presentation) to a near-normal state (LVEF of 40% or greater, and a 10% increase or greater in absolute value) were monitored for recurrence of LV systolic dysfunction. Patients with significant coronary artery disease were excluded. Patients were monitored for 41.0+/-26.3 months after recovery (LVEF 53.4+/-7.6%) from LV dysfunction. RESULTS: LV systolic dysfunction reappeared (LVEF 27.5+/-8.1%) during the follow-up period in eight of 42 patients (19.0%). No significant difference between the groups with or without recurrent heart failure was observed in the baseline clinical and echocardiographic characteristics. However, more patients in the recurred IDCMP group than those in the group that maintained the recovery state had discontinued antiheart failure medication (62.5% versus 5.9%, P<0.05). CONCLUSIONS: LV dysfunction recurs in some patients with reversible IDCMP. The recurrence was significantly correlated with the discontinuation of antiheart failure drugs. The results suggest that continuous medical therapy may be mandatory in patients who recover from LV systolic dysfunction.ope

A Case of Cephalosporin-induced DRESS (Drug Rash with Eosinophilia and Systemic Symptoms) Syndrome with Acute Renal Failure

Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome, a kind of hypersensitivity syndrome, is a life-threatening condition with various clinical manifestations such as fever, skin rash, lymph node enlargement and internal organ involvement. We report a case of skin rash and eosinophilia followed by acute renal failure and mild hepatitis after cephalosporin administration.ope

Transforming growth factor-β 기능 억제가 장기간의 고강도 운동을 수행하는 백서 심근 섬유화 감소에 미치는 역할

Dept. of Medicine/박사Background: Long-term intensive exercise training induces myocardial fibrosis, which acts as an arrhythmogenic substrate. Transforming growth factor (TGF)-β pathway causes myocardial fibrosis in various cardiac diseases. The purposes of this study were to: 1) confirm vigorous exercise-induced cardiac fibrosis and 2) examine the effect of TGF-β function blocking on cardiac structure/function and pathologic collagen deposition in a chronic intensive exercise rat model. Methods: Male Wistar rats weighing 100 to 125 g were randomly assigned to three groups: time-matched sedentary control (S-control, n=10), exercise+dimethyl sulfoxide (DMSO) [exercise control (E-control, n=5; one dropped out)] and exercise+TGF-β antagonist (TGF-β function blocking group, n=5). The exercise groups performed intensive exercise on a treadmill for 12 weeks after two weeks of conditioning. Transthoracic echocardiography was performed at the beginning and at the endpoint of exercise training under anesthesia. At the endpoint, the hearts were harvested after euthanasia and weighed. Collagen deposition in all cardiac chambers was quantified after Masson’s Trichrome stain. Biochemical studies [ribonucleic acid (RNA) of TGF-β1, fibronectin-1, matrix metalloproteinase-2 (MMP-2), of tissue inhibitors of metalloproteinase-1 (TIMP-1), collagen-Ia1, -Ia2 and –IIIa1 in all four cardiac chambers] for pathologic collagen deposition were performed with real-time polymerase chain reaction. Results: Chronic intensive exercise training (the E-control and TGF-β function blocking group) results in less increase in body weight and left ventricular (LV) wall thickening and dilation (p<0.05 for all) without significant change in ejection fraction or heart weight compared with the S-control group. Myocardial fibrosis quantity significantly increased in all cardiac chambers in the E-control group (p<0.001 compared to S-control). Of note, in the TGF-β function blocking group, pathologic collagen deposition was significantly lower than the E-control group (p<0.001) in all cardiac chambers. RNA analysis results were variable: TGF-β did not differ significantly among the three groups; MMP-2 values from left ventricle (LV) and right atrium (RA) were significantly lower in the S-control compared with the E-control (p<0.001 in LV and p=0.006 in RA) and TGF-β function blocking group (p=0.005 in LV and p=0.006 in RA), whereas other values were did not differ in intergroup comparison. Figronectin-1 values were similar in all cardiac chambers and TIMP values from LV and RA were significantly lower in the S-control group than the E-control (p=0.020 in LV and p=0.002 in RA) and TGF-β function blocking group (p=0.045 in LV and p=0.004 in RA), while other values were not remarkable. Collagen-Ia1, -Ia2 and IIIa1 values from LV and RA were significantly lower in the S-control group than the E-control group (p=0.019, p<0.001 and p=0.005 for LV and p=0.004, p<0.001 and p=0.010 for RA, respectively). When comparing values between the E-control and TGF-β function blocking group, no collagen subtypes differed significantly. Comparing the S-control and TGF-β function blocking group, collagen-Ia1 from RA (p=0.005), collagen-Ia2 from RA (p=0.001) and collagen-IIIa1 from LV (p=0.010) were significantly lower. Conclusion: TGF-β function blocking ameliorates the heart fibrosis induced by long-term intensive exercise training in animals, without impact on cardiac structure and function. 서론: 장기간 수행하는 고강도 운동이 심장 부정맥을 유발하는 심근 섬유화와 연관이 있다는 임상적, 역학적 관찰 결과들이 최근 보고되고 있다. 한편, transforming growth factor (TGF)-β pathway 는 여러 심장 질환에서 심근 섬유화에 중대한 역할을 한다. 본 연구의 목적은: 1) 고강도 운동 유발성 심근 섬유화의 발생을 백서 모델에서 확인하고, 2) 그러한 모델에서 TGF-β 의 기능 억제가 심장의 구조와 기능 및 병적인 심근 섬유화의 감소에 영향을 줄 수 있는지 확인하는 것이다. 방법: 몸무게 100~125 g 의 백서 (Wistar rat) 를 무작위로 3군으로 배정하였다: 시간 통제의 무운동 대조군 (n=10), dimethyl sulfoxide (DMSO) 를 위약으로 투여한 운동 대조군 (n=5, 1 마리 중도 탈락) 및 TGF-β 길항제를 투여한 운동 실험군 (n=5). 운동을 시행한 군들은 2주간의 적응기간을 거친 후 트레드밀에서 12주간 36 m/s 의 속도로 ...ope

Clinical fate and its contributing factors of reversible non-ischemic left ventricular systolic dysfunction

의학과/석사[한글] 연구배경: 임상적으로 비 허혈성 좌심부전이 가역적으로 회복되는 경우를 간혹 관찰할 수 있다. 하지만 이렇게 회복된 상태의 울혈성 심부전의 임상적 경과에 대한 연구는 미흡한 실정이다. 본 연구에서는 심부전에 대한 적절한 치료 후 가역적으로 회복된 비 허혈성 좌심부전 환자들을 대상으로, 울혈성 심부전이 임상적으로 회복되고 좌심실 구혈률이 정상화 되더라도, 재발성 좌심부전이 발생할 가능성이 있다는 가정 하에 이들의 임상적 경과와 이에 영향을 미치는 요인들을 조사하였다.재료 및 방법: 임상적 평가와 심 초음파 소견 상 가역적 회복을 보인 비 허혈성 좌심부전 환자 50명을 대상으로 하였다. 이들은 심부전의 최초 진단 시 NYHA(New York Heart Association) class가 III 혹은 IV였으며, 심 초음파상 좌심실 구혈률은 40% 미만이었고, 전체 추적 관찰 기간은 48.4±15.3개월이었다. 이들 중 남자는 32명, 여자는 18명이었고 나이는 54.9±12.4세 였으며, 최초 진단 시 좌심실 구혈률을 28.8±7.2% 였다. 울혈성 심부전의 원인 질환으로는 특발성 확장성 심근증이 39명으로 가장 많았고, 이외에 알콜에 의한 확장성 심근증 7명, 아드리아마이신에 의한 확장성 심근증이 2명, 빈맥에 의한 심근증이 2명이었다. 이들은 심부전에 대한 적절한 치료를 시작하고 나서 16.9±13.9개월 만에 좌심실 구혈률이 개선되었으며(좌심실 구혈률>40% 및 절대적으로 10% 이상의 개선) 심부전의 증상은 모두 호전되었고, 이후 27.1±2.9개월간 추적 관찰하였다. 하지만 모두 9명의 환자에게서 46.6±31.7개월 만에 좌심 기능의 재 악화가 발생하였는데, 이들 중 5명은 심부전의 회복 후 항 심부전 약물을 중단한 환자들이었다. 좌심 기능의 재 악화에는 항 심부전 약물의 중단 여부가 통계적으로 유의한 요인으로 작용하였다.결론: 가역적으로 회복된 비 허혈성 좌심부전 환자들은, 좌심 기능의 재 악화에 따른 재발성 심부전이 발생할 가능성이 있으므로, 추적 관찰이 필요하며, 또한 좌심 기능의 회복 후에도 항 심부전 약물의 지속적 투여가 필요할 것으로 생각된다. [영문]Background: Non-ischemic left ventricular systolic dysfunction is known to recover in some cases with reversible feature, but our knowledge about the clinical fate and consequences of recovered heart failure is limited. We hypothesized that although left ventricular ejection fraction normalizes and clinical features of congestive heart failure are clinically recovered after appropriate treatment in patients with non-ischemic heart failure, some of them may have deleterious consequences due to recurrent LV systolic dysfunction and heart failure.Methods and Results: Fifty patients, who revealed reversible left ventricular sys- tolic dysfunction by echocardiography and clinically recovered from heart failure were enrolled. All had NYHA(New York Heart Association) functional class III heart failure or greater and ejection fraction less than 40% measured by echocardiography on initial presentation and mean follow up period was 48.4±15.3 months. There were 32 men and 18 women with mean age of 54.9±12.4 years and initial left ventricular ejection fraction of 28.8±7.2%. The cause of congestive heart failure was idiopathic dilated cardiomyopathy(n=39), alcohol induced dilated cardiomyopathy (n=7), adriamycin induced dilated cardiomyopathy(n=2), tachycardia induced cardiom- yopathy(n=2). After 16.9±13.9 months of treatment left ventricular ejection fraction improved or normalized(ejection fraction>40% and at least 10% of improvement absolutely) and symptoms abated all. But, 9 patients had recurred congestive heart failure due to decrease left ventricular systolic function after 46.6±31.7 months and 5 of them had been stopped anti-heart failure medication. Cessation of anti-heart failure medication was statistically significant influencing factor in recurrent heart failure patient.Conclusion: In patients with reversible non-ischemic left ventricular systolic dys- function, recurrent heart failure may ensue, so close follow up is needed. The main- tenance of anti-heart failure medication is thought to be a significant influencing factor of those clinical consequences.ope

Left ventricular hypertrophy determines the severity of diastolic dysfunction in patients with nonvalvular atrial fibrillation and preserved left ventricular systolic function

Regression of left ventricular (LV) hypertrophy (LVH) is known to be related to a lower incidence of stroke in hypertensive patients with nonvalvular atrial fibrillation (NV-AF). However, its mechanism remains controversial. Recently, diastolic dysfunction (DD) was reported to be correlated with ischemic stroke in NV-AF. We hypothesized that hypertension (HTN) and resultant LVH might be associated with the severity of DD in NV-AF. Two hundred and ninety-four patients (204 males, age 66 ± 12 y) with NV-AF with preserved LV systolic function were included. Clinical and echocardiographic data were compared between patients with enlarged left atrial (LA) volume (n = 237) and patients with normal LA. Age (60 ± 12 vs. 67 ± 11 years), sex (male; 81 vs. 62%), duration of NV-AF (4.1 ± 7.8 vs. 45.7 ± 49.0 months), brain natriuretic peptide (108.3 ± 129.3 vs. 236.1 ± 197.0 pg/mL), right ventricular systolic pressure (24.5 ± 5.5 vs. 33.1 ± 11.1 mmHg), mitral inflow velocity (E [77.4 ± 22.2 vs. 88.3 ± 22.0 cm/s]), LV mass index (LVMI [87.6 ± 22.2 vs. 105.1 ± 23.2 g/m(2)]), peak systolic mitral annular velocity (S' [7.2 ± 2.0 vs. 5.8 ± 1.8 cm/s]), and mitral inflow velocity to diastolic mitral annular velocity (E/E' [9.8 ± 3.4 vs. 12.1 ± 4.4]) were significantly different between the two groups, respectively (P < 0.05). In multivariate analysis, LVMI was independently correlated with increased LA volume (OR: 1.037 [95% CI: 1.011-1.063], P < 0.05), whereas HTN was not. LA enlargement, which reflects the severity and chronicity of DD, is independently associated with LVH in patients with NV-AF. Therefore, regression of LVH with anti-hypertensive treatment may lead to improvement of diastolic function and favorable clinical outcomes in hypertensive patients with NV-AF.ope

Central aortic pressure in aortic aneurysm and aortic dissection: a novel prognostic marker

BACKGROUND: Some aortic aneurysm (AA) or aortic dissection (AD) patients can be observed to detect disease progression if optimal blood pressure is achieved. However, in another group of patients, disease progression occurs despite well-controlled blood pressure. The aim of this study was to determine the prognostic value of central aortic pressure in AA and AD. METHODS: Fifty-six newly diagnosed AA or AD patients (37 men, age: 60.3 +/- 12.9 years) who did not need urgent surgery or interventional treatment were enrolled. All patients achieved brachial SBP < or = 120 mm Hg with beta-blocker-based treatment within 1 month. Then, central aortic pressure parameters were noninvasively checked with radial tonometry (SphygmoCor Px Pulse Wave Analysis System, AtCor Medical, Sydney, Australia). All patients were monitored for at least 6 months and for up to 5 years. RESULTS: Thirty-three patients did well without disease progression. However, disease progression was noted despite well-controlled brachial blood pressure in 23 patients. In intergroup comparisons, central aortic systolic pressure (112.7 +/- 3.5 mm Hg vs. 104.3 +/- 7.5 mm Hg) and aortic augmentation index (AI: 33.4 +/- 13.5% vs. 23.4 +/- 8.7%) were significantly high in the disease progression group (P < 0.05). CONCLUSION: In some AA or AD patients, central aortic pressure and AI can be considered as surrogate prognostic markers.ope

Abnormal myocardial capillary density in apical hypertrophic cardiomyopathy can be assessed by myocardial contrast echocardiography.

BACKGROUND: Myocardial ischemia and dysfunction can occur in hypertrophic cardiomyopathy (HCM) because of the high muscle-to-blood ratio, even without significant coronary artery disease. Microbubbles reside only in the intravascular space and myocardial video-intensity during systole results mostly from microbubbles within capillaries. The hypothesis explored in the present study was that an abnormal capillary density in apical HCM (ApHCM) can be demonstrated using myocardial contrast echocardiography (MCE). METHODS AND RESULTS: The 56 patients were investigated (31 males, age 58 ± 9 years; 33 ApHCM, 9 hypertensive left ventricular hypertrophy [LVH], 14 controls). MCE was performed with low-mechanical-index power modulation imaging. Tissue Doppler imaging to assess myocardial contractile function was obtained at the mitral annulus (S'), and (99 m)Tc-MIBI SPECT was also performed. All ApHCM patients exhibited perfusion defects at the hypertrophied segments in the systolic phase during MCE, whereas SPECT showed normal or rather increased perfusion at those sites. The cyclic variation of video-intensity was exaggerated in ApHCM when compared with the LVH or control group (% of [systolic video-intensity]/[diastolic video-intensity]: 33.0 ± 12.3%, 88.3 ± 19.2% and 79.4 ± 13.9%, respectively [P<0.05]). Concurrently, MCE cyclic variation and perfusion defect size were related to decreased S' (P<0.05 for all). CONCLUSIONS: A perfusion defect at the hypertrophied segment, representing abnormal myocardial capillary density, was observed in ApHCM patients during MCE. The extent of MCE cyclic variation and the perfusion defect size both correlate with decreased myocardial contractile property in ApHCM.ope

Different clinical outcome of paravalvular leakage after aortic or mitral valve replacement.

Although aortic valve replacement (AVR) and mitral valve replacement (MVR) are the most commonly performed prosthetic valve replacement operations, it is unclear whether clinical outcomes of paravalvular leakage (PVL) after MVR or AVR are different. It was hypothesized that clinical outcomes of PVL after AVR would be more favorable than after MVR because the pressure gradient is much larger in PVL occurring at the mitral position, which happens at the systolic phase, than at the aortic valve. Over a 12-year period, 82 patients with PVL were identified. After excluding patients who required immediate surgical repair for severe symptoms, patients with Behçet disease or infective endocarditis, and those with PVL involving both valves, 54 remaining patients (21 women, mean age 56 ± 14 years, 23 AVRs) with mild to moderate leakage constituted the study population. The end points were cardiac death, all-cause mortality, repeat surgery, and urgent admission for heart failure. During a median follow-up period of 35 months, there were 27 events, including 23 repeated surgeries, 2 cardiac deaths, 1 noncardiac death, and 1 admission for heart failure. Cox regression analysis revealed that the valve location of PVL was the only independent clinical predictor of event-free survival. The estimated 8-year event-free survival rate was significantly higher in patients with PVL after AVR than those after MVR (70 ± 12% vs 16 ± 8%, p <0.0001). In conclusion, PVL after AVR demonstrated more favorable long-term clinical outcomes compared to that after MVR. In patients who develop PVL after AVR, repeat surgery may be deferred. However, in patients with PVL after MVR, more aggressive therapeutic approaches should be considered.ope