Surgically Metabolic Resection of Pericardial Fat to Ameliorate Myocardial Mitochondrial Dysfunction in Acute Myocardial Infarction Obese Rats

Background@#Pericardial fat (PF) is highly associated with cardiovascular disease but the effectiveness of surgical resection of PF is still unknown for myocardial mitochondrial structure and function in acute myocardial infarction (AMI) with obesity. The aim of this study was to demonstrate the difference in myocardial mitochondrial structure and function between obese AMI with additionally resected PF and those without resected PF. @*Methods@#Obese rats with 12-week high fat diet (45 kcal% fat, n = 21) were randomly assigned into 3 groups: obese control, obese AMI and obese AMI with additionally resected PF. One week after developing AMI and additional resection of PF, echocardiogram, myocardial mitochondrial histomorphology, oxidative phosphorylation system (OXPHOS), anti-oxidative enzyme and sarcoplasmic reticulum Ca 2+ ATPase 2 (SERCA2) in the non-infarcted area were assessed between these groups. @*Results@#There was significant improvement of systolic function in AMI with PF resection compared with the AMI group in the echocardiogram. Even though the electron microscopic morphology for the mitochondria seems to be similar between the AMI with PF resection and AMI groups, there was an improved expression of PGC-1α and responsive OXPHOS including NDUFB3, NDUFB5 and SDHB are associated with the ATP levels in the AMI with PF resection compared with those in the AMI group. In addition, the expression levels of antioxidant enzymes (MnSOD) and SERCA2 were improved in the AMI with PF resection compared with those in the AMI group. @*Conclusion@#Surgical resection of PF might ameliorate myocardial mitochondria dysfunction in obese AMI.

Application of Animal Models in Diabetic Cardiomyopathy

Diabetic heart disease is a growing and important public health risk. Apart from the risk of coronary artery disease or hypertension, diabetes mellitus (DM) is a well-known risk factor for heart failure in the form of diabetic cardiomyopathy (DiaCM). Currently, DiaCM is defined as myocardial dysfunction in patients with DM in the absence of coronary artery disease and hypertension. The underlying pathomechanism of DiaCM is partially understood, but accumulating evidence suggests that metabolic derangements, oxidative stress, increased myocardial fibrosis and hypertrophy, inflammation, enhanced apoptosis, impaired intracellular calcium handling, activation of the renin-angiotensin-aldosterone system, mitochondrial dysfunction, and dysregulation of microRNAs, among other factors, are involved. Numerous animal models have been used to investigate the pathomechanisms of DiaCM. Despite some limitations, animal models for DiaCM have greatly advanced our understanding of pathomechanisms and have helped in the development of successful disease management strategies. In this review, we summarize the current pathomechanisms of DiaCM and provide animal models for DiaCM according to its pathomechanisms, which may contribute to broadening our understanding of the underlying mechanisms and facilitating the identification of possible new therapeutic targets.

Application of Animal Models in Diabetic Cardiomyopathy

Diabetic heart disease is a growing and important public health risk. Apart from the risk of coronary artery disease or hypertension, diabetes mellitus (DM) is a well-known risk factor for heart failure in the form of diabetic cardiomyopathy (DiaCM). Currently, DiaCM is defined as myocardial dysfunction in patients with DM in the absence of coronary artery disease and hypertension. The underlying pathomechanism of DiaCM is partially understood, but accumulating evidence suggests that metabolic derangements, oxidative stress, increased myocardial fibrosis and hypertrophy, inflammation, enhanced apoptosis, impaired intracellular calcium handling, activation of the renin-angiotensin-aldosterone system, mitochondrial dysfunction, and dysregulation of microRNAs, among other factors, are involved. Numerous animal models have been used to investigate the pathomechanisms of DiaCM. Despite some limitations, animal models for DiaCM have greatly advanced our understanding of pathomechanisms and have helped in the development of successful disease management strategies. In this review, we summarize the current pathomechanisms of DiaCM and provide animal models for DiaCM according to its pathomechanisms, which may contribute to broadening our understanding of the underlying mechanisms and facilitating the identification of possible new therapeutic targets.

Diabetic cardiomyopathy: where we are and where we are going

The global burden of diabetes mellitus and its related complications are currently increasing. Diabetes mellitus affects the heart through various mechanisms including microvascular impairment, metabolic disturbance, subcellular component abnormalities, cardiac autonomic dysfunction, and a maladaptive immune response. Eventually, diabetes mellitus can cause functional and structural changes in the myocardium without coronary artery disease, a disorder known as diabetic cardiomyopathy (DCM). There are many diagnostic tools and management options for DCM, although it is difficult to detect its development and effectively prevent its progression. In this review, we summarize the current research regarding the pathophysiology and pathogenesis of DCM. Moreover, we discuss emerging diagnostic evaluation methods and treatment strategies for DCM, which may help our understanding of its underlying mechanisms and facilitate the identification of possible new therapeutic targets.

Effect of Long-term Fenofibrate Therapy on Serum Creatinine and Its Reversibility in Hypertriglyceridemic Patients with Hypertension

OBJECTIVE: Previous studies have shown that fenofibrate therapy increases serum creatinine level and that there is a return of serum creatinine to baseline level after the discontinuation of the drug. We evaluated the effect of long-term fenofibrate therapy on creatinine levels and its reversibility in patients with hypertension and hypertriglyceridemia. METHODS: This retrospective study enrolled 54 hypertensive and hypertriglyceridemic patients taking fenofibrate for 3–6 years (Fenofibrate group) and 30 control patients with similar age, sex, follow-up duration, and creatinine levels (Control group). In 23 patients taking fenofibrate with low triglyceride level and/or with high creatinine levels, fenofibrate was discontinued, and creatinine levels were measured after 2 months. RESULTS: Creatinine levels increased in both the fenofibrate group (from 0.91±0.18 mg/dL to 1.09±0.23 mg/dL, p < 0.001) and the control group (from 0.94±0.16 mg/dL to 0.98±0.16 mg/dL, p=0.04) compared to baseline. However, the elevation was more pronounced in the fenofibrate group than in the control group (21.1±15.4% vs. 4.5±11.3%, p < 0.001). The discontinuation of fenofibrate lowered creatinine levels (from 1.39±0.32 mg/dL to 1.15±0.24 mg/dL, p < 0.001) which were still higher than pre-treatment levels (p=0.013). CONCLUSION: Long-term fenofibrate therapy significantly increased creatinine levels in hypertensive and hypertriglyceridemic patients. The effect of fenofibrate on creatinine level was partially reversible. This finding suggests that follow-up creatinine level is necessary with fenofibrate therapy.

Multimodality Intravascular Imaging Assessment of Plaque Erosion versus Plaque Rupture in Patients with Acute Coronary Syndrome

BACKGROUND AND OBJECTIVES: We assessed plaque erosion of culprit lesions in patients with acute coronary syndrome in real world practice. SUBJECTS AND METHODS: Culprit lesion plaque rupture or plaque erosion was diagnosed with optical coherence tomography (OCT). Intravascular ultrasound (IVUS) was used to determine arterial remodeling. Positive remodeling was defined as a remodeling index (lesion/reference EEM [external elastic membrane area) >1.05. RESULTS: A total of 90 patients who had plaque rupture showing fibrous-cap discontinuity and ruptured cavity were enrolled. 36 patients showed definite OCT-plaque erosion, while 7 patients had probable OCT-plaque erosion. Overall, 26% (11/43) of definite/probable plaque erosion had non-ST elevation myocardial infarction (NSTEMI) while 35% (15/43) had ST elevation myocardial infarction (STEMI). Conversely, 14.5% (13/90) of plaque rupture had NSTEMI while 71% (64/90) had STEMI (p<0.0001). Among plaque erosion, white thrombus was seen in 55.8% (24/43) of patients and red thrombus in 27.9% (12/43) of patients. Compared to plaque erosion, plaque rupture more often showed positive remodeling (p=0.003) with a larger necrotic core area examined by virtual histology (VH)-IVUS, while negative remodeling was prominent in plaque erosion. Overall, 65% 28/43 of plaque erosions were located in the proximal 30 mm of a culprit vessel-similar to plaque ruptures (72%, 65/90, p=0.29). CONCLUSION: Although most of plaque erosions show nearly normal coronary angiogram, modest plaque burden with negative remodeling and an uncommon fibroatheroma might be the nature of plaque erosion. Multimodality intravascular imaging with OCT and VH-IVUS showed fundamentally different pathoanatomic substrates underlying plaque rupture and erosion.

Effect of Short-term Fenofibrate Therapy on Blood Creatinine Levels in Patients with Hypertriglyceridemia / 대한내과학회지

BACKGROUND/AIMS: Previous studies have reported that fenofibrate therapy increases blood creatinine levels. The aim of this study was to evaluate the effect of fenofibrate therapy on the renal function in patients with hypertriglyceridemia and to determine the parameters associated with changes in renal functions. METHODS: This prospective study enrolled 86 hypertriglyceridemic patients (triglycerides > or = 200 mg/dL) who were divided into two groups: the fenofibrate group (n = 43), who received 160 mg of fenofibrate, and the control group (n = 43). Lipid profiles and renal function were measured at the beginning of the study and after 2 months. RESULTS: The estimated glomerular filtration rate (eGFR) decreased in the fenofibrate group (p < 0.001), but did not change in the control group (p = 0.80). Accordingly, the decrease was more pronounced in the fenofibrate group than the control group (-18.6 +/- 8.6 vs. 0.9 +/- 9.6%, respectively; p < 0.001). Changes in serum creatinine (p < 0.001) and blood urea nitrogen (p < 0.005) levels were similar to those of eGFR. In a stepwise linear regression analysis, the percent change in creatinine was independently associated with fenofibrate therapy (r = 0.71; p < 0.001) and old age (r = 0.27; p < 0.05) in all patients. In the fenofibrate group, percent change in creatinine was associated with age (r = -0.51; p < 0.001) and smoking (r = 0.42; p < 0.005), while percent change was associated with body mass index (r = 0.31; p < 0.05) in the control group. Elevation of creatinine by 20% or more was associated with fenofibrate therapy (p < 0.001) and old age (p < 0.005) in all patients, and with old age (p < 0.001) in the fenofibrate group. CONCLUSIONS: Short-term fenofibrate therapy significantly impaired the renal function of hypertriglyceridemic patients, and this effect was more pronounced in elderly patients. This finding suggests that creatinine levels should be followed in patients receiving fenofibrate therapy.

Influence of Previous Statin Therapy on Cholesterol-Lowering Effect of Ezetimibe

BACKGROUND AND OBJECTIVES: The inhibition of cholesterol absorption by ezetimibe increases cholesterol synthesis. The effect of inhibition of cholesterol synthesis on cholesterol absorption is controversial. The influence of these interactions on cholesterol levels is unknown. We investigated on the extent to which cholesterol levels were affected by the reaction of one pathway to the inhibition of the other pathway. SUBJECTS AND METHODS: This case-controlled study enrolled 198 patients who needed cholesterol-lowering drugs. Ezetimibe (10 mg) was administered to the patients with (n=58) and without on-going statin therapy (n=58). Simvastatin (20 mg) was administered to the patients treated with (n=41) and without ezetimibe (n=41). RESULTS: Ezetimibe without statin lowered the total cholesterol by 13.3+/-8.8% (p<0.001) and the low density lipoprotein-cholesterol (LDL-C) by 18.7+/-15.3% (p<0.001). Ezetimibe added to statin decreased the total cholesterol by 21.1+/-7.7% (p<0.001) and the LDL-C by 29.9+/-12.6% (p<0.001). The total cholesterol and LDL-C were reduced more by ezetimibe in patients with statin therapy than in those without statin therapy (p<0.001 and p<0.001, respectively). The differences in the effect of simvastatin on total cholesterol and LDL-C between the patients with and without ezetimibe showed borderline significance (p=0.10 and p=0.055, respectively). CONCLUSION: A prior inhibition of cholesterol synthesis by statin enhanced the effect of ezetimibe on total cholesterol and LDL-C by 7.8% and 11.2%, respectively. This finding suggests that ezetimibe increased cholesterol synthesis, resulting in a significant elevation of cholesterol levels.

Effect of Fenofibrate Therapy on Blood Creatinine Levels in Patients with Hypertension and Hypertriglyceridemia

OBJECTIVE: Previous studies have reported that fenofibrate therapy increased blood creatinine levels. We investigated the effect of fenofibrate therapy on creatinine levels in patients with hypertension and hypertriglyceridemia. METHODS: This retrospective study included 36 hypertensive patients with hypertriglyceridemia taking fenofibrate for 1-3 years (Fenofibrate group) and 36 control patients with similar age, sex, follow-up duration, creatinine levels, and lipid levels to those of fenofibrate therapy (Control group). RESULTS: Baseline parameters except lipid profiles were similar between the fenofibrate and control groups. Creatinine levels increased in the fenofibrate group (from 0.90+/-0.18 mg/dL to 1.05+/-0.22 mg/dL, p<0.001) and did not change in the control group (from 0.91+/-0.12 mg/dL to 0.92+/-0.14 mg/dL, p=0.39). The elevation was more pronounced in the fenofibrate group than in the control group (0.15+/-0.12 vs. 0.02+/-0.11 mg/dL, p<0.001). Changes in creatinine levels were only associated with fenofibrate therapy (r=0.52, p<0.001) in the stepwise linear regression analysis. CONCLUSION: Fenofibrate therapy for 1-3 years significantly increased creatinine levels in hypertensive patients with hypertriglyceridemia. This finding suggests that follow-up measurement of creatinine level is necessary with fenofibrate therapy.

Acute Viral Myopericarditis Presenting as a Transient Effusive-Constrictive Pericarditis Caused by Coinfection with Coxsackieviruses A4 and B3

Acute myopericarditis is usually caused by viral infections, and the most common cause of viral myopericarditis is coxsackieviruses. Diagnosis of myopericarditis is made based on clinical manifestations of myocardial (such as myocardial dysfunction and elevated serum cardiac enzyme levels) and pericardial (such as inflammatory pericardial effusion) involvement. Although endomyocardial biopsy is the gold standard for the confirmation of viral infection, serologic tests can be helpful. Conservative management is the mainstay of treatment in acute myopericarditis. We report here a case of a 24-year-old man with acute myopericarditis who presented with transient effusive-constrictive pericarditis. Echocardiography showed transient pericardial effusion with constrictive physiology and global regional wall motion abnormalities of the left ventricle. The patient also had an elevated serum troponin I level. A computed tomogram of the chest showed pericardial and pleural effusion, which resolved after 2 weeks of supportive treatment. Serologic testing revealed coxsackievirus A4 and B3 coinfection. The patient received conservative medical treatment, including nonsteroidal anti-inflammatory drugs, and he recovered completely with no complications.

Relation Between RR Intervals and Early Diastolic Mitral Annular Velocities in Atrial Fibrillation

BACKGROUND AND OBJECTIVES: Irregular RR intervals in atrial fibrillation (AF) make beat-to-beat changes in left ventricular (LV) systolic performance. Early diastolic mitral annular velocity (E') is one of the well-established parameters for evaluating LV diastolic function. The relation between RR intervals and E's is unknown. The aim of this study was to observe the influence of continuous changes in RR interval on the parameter for diastolic function in AF. SUBJECTS AND METHODS: Echocardiography was performed in 117 patients with AF. E' was adjusted for the effect of pre-preceding RR interval (RR-2) using the logarithmic equation between RR-2 and E'. The logarithmic equation between adjusted E' and preceding RR interval (RR-1) was calculated. RESULTS: The slope in the relation between RR-1 and E' varied from -2.5 to 2.6. The slope was lower (more likely negative) in patients with higher ratio of early diastolic mitral flow velocity (E) to E' (r=-0.21, p=0.023), ischemic heart disease (IHD, r=0.21, p=0.026), and higher systolic blood pressure (r=-0.19, p=0.046). When patients were divided into these 3 groups on the basis of slope, the lowest slope group (0.57, n=39). The slope with regards to the relationship between RR-2 and E' also varied from -3.4 to 3.1. CONCLUSION: Changes in RR intervals had variable effects on E's according to clinical variables in AF.

Effect of Statins on C-reactive Protein, Lipoprotein(a) and Fibrinogen in Hypercholesterolemic Patients

OBJECTIVE: C-reactive protein (CRP), lipoprotein (a)[Lp(a)], and fibrinogen are associated with systemic inflammatory reactions. Statins have anti-inflammatory effects. However, the effect of statins on these parameters is inconsistent. We evaluated the effect of statins on inflammatory markers and variables related to changes in these markers. METHODS: A total of 390 hypercholesterolemic patients were enrolled. Atorvastatin (n=112), lovastatin (n=25), pitavastatin (n=49), rosuvastatin (n=20), and simvastatin (n=184) were administered. Lipids, CRP, Lp(a), and fibrinogen levels were measured before and after 2 months of the therapy. RESULTS: Statins reduced cholesterol, low density lipoprotein (LDL) cholesterol, and triglyceride levels by -28.9+/-9.1% (P=0.000), -41.4+/-12.4% (P=0.000), and -11.6+/-39.4% (P=0.000), respectively and increased high density lipoprotein (HDL) cholesterol level by 2.56+/-13.2% (P=0.014). CRP levels decreased from 1.23+/-1.30 to 1.14+/-1.29 mg/L (P=0.000). Lp(a) levels were not changed (P=0.91) and fibrinogen levels increased from 277.8+/-54.4 to 282.6+/-56.9 mg/dL (P=0.042). Changes in CRP levels were associated with baseline CRP levels (r=-0.56, P=0.000) and changes in HDL cholesterol levels (r=-0.14, P=0.005). Changes in Lp(a) levels were associated with changes in triglyceride (r=-0.24, P=0.000) and baseline aspartate aminotransferase level (r=0.12, P=0.015). Changes in fibrinogen levels were associated with baseline fibrinogen levels (r=-0.40, P=0.000), sex (r=0.18, P=0.001), and changes in HDL cholesterol levels (r=-0.15, P=0.003). CONCLUSION: Inflammatory markers showed different responses to statins and changes in these markers were associated with different parameters. This finding suggests that anti-inflammatory effect of statin is confined to a specific pathway of inflammation.

Fenofibrate Reduces C-Reactive Protein Levels in Hypertriglyceridemic Patients With High Risks for Cardiovascular Diseases

BACKGROUND AND OBJECTIVES: The effects of fenofibrate on C-reactive protein (CRP) are under debate. We investigated the effect of fenofibrate on CRP levels and the variables determining changes. SUBJECTS AND METHODS: This case-control study enrolled 280 hypertriglyceridemic patients who were managed either with 200 mg of fenofibrate (Fenofibrate group, n=140) or with standard treatment (comparison group, n=140). CRP levels were measured before and after management for 2 months. RESULTS: CRP levels decreased in both the fenofibrate (p=0.003) and comparison (p=0.048) groups. Changes in CRP levels were not significantly different between the two groups (p=0.27) and were negatively associated with baseline CRP levels (r=-0.47, p or =1 mg/L, CRP levels also decreased in both groups (p=0.000 and p=0.001 respectively), however, more in the fenofibrate group than in the comparison group (p=0.025). The reduction of CRP was associated with higher baseline CRP levels (r=-0.29, p=0.001), lower body mass index (BMI, r=0.23, p=0.007), and fenofibrate therapy (r=0.19, p=0.025). CRP levels decreased more in the fenofibrate group than in the comparison group in patients with a BMI < or =26 kg/m2 with borderline significance (-1.21+/-1.82 mg/L vs. -0.89+/-1.92 mg/L, p=0.097). In patients with a high density lipoprotein-cholesterol level <40 mg/dL, CRP levels were reduced only in the fenofibrate group (p=0.006). CONCLUSION: Fenofibrate reduced CRP levels in hypertriglyceridemic patients with high CRP and/or low high density lipoprotein-cholesterol levels and without severe overweight. This finding suggests that fenofibrate may have an anti-inflammatory effect in selected patients.

Spontaneous Spinal Epidural Hematomas Associated With Acute Myocardial Infarction Treatment

Many studies have reported spontaneous spinal epidural hematoma (SSEH). Although most cases are idiopathic, several are associated with thrombolytic therapy or anticoagulants. We report a case of SSEH coincident with acute myocardial infarction (AMI), which caused serious neurological deficits. A 56 year old man presented with chest pain accompanied with back and neck pain, which was regarded as an atypical symptom of AMI. He was treated with nitroglycerin, aspirin, low molecular weight heparin, and clopidogrel. A spinal magnetic resonance image taken after paraplegia developed 3 days after the initial symptoms revealed an epidural hematoma at the cervical and thoracolumbar spine. Despite emergent decompressive surgery, paraplegia has not improved 7 months after surgery. A SSEH should be considered when patients complain of abrupt, strong, and non-traumatic back and neck pain, particularly if they have no spinal pain history.

Effects of the Transition from Premenopause to Postmenopause on Lipids and Lipoproteins: Quantification and Related Parameters

BACKGROUND/AIMS: The aim of this study was to quantitatively measure changes in lipids and lipoproteins during perimenopause and to identify variables related to these changes. METHODS: Among women who had three regular health evaluations over a span of 2-4 years, 34 women remained in the premenopausal state, 34 premenopausal women transitioned to the postmenopausal state, and 36 postmenopausal women were enrolled. The menopausal state was determined not only by a history of amenorrhea but also by levels of female sex hormones. Yearly changes in lipids were calculated using a linear regression of the three measurements. RESULTS: The transition from premenopause to postmenopause was associated with increased total cholesterol and low-density lipoprotein (LDL) cholesterol levels by 7.4 +/- 8.0 mg/dL (4.2 +/- 4.9%) and 6.9 +/- 6.5 mg/dL (6.8 +/- 7.0%) over one year, resulting in an elevation of 19.6 +/- 22.6 mg/dL (10.9 +/- 13.0%) and 18.9 +/- 19.5 mg/dL (18.6 +/- 20.3%), respectively, during perimenopause. There were no changes observed in premenopausal and postmenopausal women. Body weight, blood pressure, high-density lipoprotein (HDL) cholesterol, and triglycerides did not change in any of the three groups. In all women, changes in both total cholesterol and LDL cholesterol were associated with changes in follicle stimulating hormone (r = 0.40, p < 0.001 and r = 0.38, p < 0.001, respectively). Changes in triglycerides were associated with changes in body weight (r = 0.28, p = 0.005). CONCLUSIONS: During perimenopause, total and LDL cholesterol levels increase and these changes in cholesterol are mainly dependent on changes in female sex hormones.

Effects of Ezetimibe Added to Ongoing Statin Therapy on C-Reactive Protein Levels in Hypercholesterolemic Patients

BACKGROUND AND OBJECTIVES: Ezetimibe alone does not decrease C-reactive protein (CRP) levels in hypercholesterolemic patients. However, several reports have suggested that ezetimibe might potentiate the effect of statin not only on cholesterol but also on CRP when administered together. We investigated the effect of ezetimibe on CRP levels in patients taking statins. SUBJECTS AND METHODS: Patients who had not achieved recommended low density lipoprotein-cholesterol (LDL-C) goals with statin therapy were divided into two groups, the ezetimibe group (n=60) and the control group (n=60). A third group of hypercholesterolemic patients without statin therapy was treated with statin (n=59). Patients with CRP level 10 mg/L were excluded. Lipid and CRP levels were measured before therapy commenced, and after 2 months of therapy. RESULTS: Ezetimibe decreased cholesterol and LDL-C levels by 20.2% (p=0.000) and 28.1% (p=0.000) respectively. However, ezetimibe did not reduce CRP levels (from 0.83+/-0.68 to 1.14+/-1.21 mg/dL, p=0.11). CRP levels remained unchanged in the control group (p=0.42). In contrast, statin lowered CRP levels (from 0.82+/-0.73 to 0.65+/-0.57 mg/dL, p=0.008). In patients taking statins, changes in CRP levels were not associated with changes in LDL-C (r=-0.02, p=0.87), but with baseline CRP levels (r=-0.38, p=0.000). CONCLUSION: Ezetimibe failed to reduce CRP levels in hypercholesterolemic patients taking statins despite significant reduction of LDL-C. This finding suggests that the anti-inflammatory effect of statin may not be secondary to cholesterol reduction, but via other mechanisms.

Is There a Benefit of Drug-Eluting Stents Rather than Bare Metal Stents in Large Coronary Artery Lesions? / 대한내과학회지

Drug-eluting stents (DES) are widely used rather than bare metal stents (BMS) in percutaneous coronary intervention (PCI) because DES have been shown to dramatically reduce restenosis and improve the rate of event free survival. Many clinical trials have been shown the advantages of DES over BMS in subset of small coronary artery diseases. There are, however, conflicting reports on the advantages of DES over BMS for larger coronary artery lesions. In this issue of the journal, Kim et al investigated the clinical outcomes between DES and BMS in large coronary artery diseases. In future, additional large, randomized, controlled, muticenter trials with new generation DES and intravascular ultrasound-guided PCI will be needed to define the clear role of DES on large coronary artery lesions.

The Impact of Mitral Annular Calcification on Left Ventricular Function in Nonagenarians

BACKGROUND AND OBJECTIVES: Mitral annular calcification (MAC) is known to be associated with degenerative processes of the cardiac fibrous skeleton and cardiovascular disease mortality. However, MAC has not been evaluated in an extreme age group (patients > or =90 years of age). In this study, the clinical significance of MAC associated with aging was examined in this age group and compared with MAC associated with aging in a younger (20 to 50 years of age) group of patients. SUBJECTS AND METHODS: We assessed echocardiographic parameters in 43 nonagenarians and 51 young patients. In the nonagenarian group, patient's age was 92+/-2 years and 27% were male; in the young control group, patient's age was 36+/-9 years and 51% were male. Comprehensive M-mode and Doppler echocardiography, including tissue Doppler imaging, were performed. The frequency and severity of MAC was assessed from the leading anterior to the trailing posterior edge at its largest width for least 3 cardiac cycles. RESULTS: Echocardiography showed that the left ventricular (LV) end-diastolic dimension was larger in the young controls (p=0.007); however, the ejection fraction (EF) was lower in the nonagenarian group (p=0.001). The frequency of MAC was greater in nonagenarians {42/43 (97%)} than in controls {9/51 (17%), p<0.0001}. The maximal width of MAC was larger in nonagenarians (0.52+/-0.17 mm and 0.05+/-0.13 mm, p<0.0001). MAC was correlated with LV mass index (g/m2) (r=0.280, p=0.014) and EF (%) (r=-0.340, p=0.001). More importantly, early mitral inflow velocity/early diastolic mitral annulus velocity (E/E') was strongly correlated with MAC in non-agenarians (r= 0.683, p<0.0001). CONCLUSION: MAC may be associated with extreme age and increased LV filling pressure in nonagenarians. Further study is necessary to assess the cardiovascular mortality and structural changes related to mitral annulus calcification associated with aging.

Progression and Observational Frequency of Atheromatous Plaques in Autopsied Coronary Arteries

BACKGROUND AND OBJECTIVES: Virtual histology-intravascular ultrasound (VH-IVUS) studies on early-stage fibroatheroma, the probable precursor lesion of progression to thin-cap fibroatheroma (TCFA), have only rarely been done in man. We investigated the progression and observational frequency of fibroatheromas, and compared plaque components between early-stage and advance-staged fibroatheromas in the general population. SUBJECTS AND METHODS: We assessed coronary fibroatheromas using VH-IVUS and histopathologic analysis of 109 coronary lesions from 40 autopsied cases that were not due to sudden cardiac death (NSCD cases). Fibroatheromas were grouped into early fibroatheroma, late fibroatheroma, thick-cap fibroatheroma (TkCFA), and thin-cap fibroatheroma. RESULTS: Mean patient age was 45+/-11 years old and 71% were males. Of 109 lesions, 27% were early fibroatheromas, 53% late fibroatheromas, 9% TkCFA, and 11% TCFA. VH-IVUS showed that there was relatively less fibrotic and fibrofatty plaque and more dense calcium deposits as fibroatheromas progressed. Furthermore, the relative amounts of fibrotic and fibrofatty plaque decreased (r=0.773, p<0.001 and r=0.538, p<0.001, respectively) as the necrotic core increased, while the relative area of dense calcium increased (r=0.665, p<0.001) as the size of the necrotic core increased. CONCLUSION: Of NSCD cases in Korea, 27% were early fibroatheromas, 53% were late fibroatheromas, 9% were TkCFA, and 11% were TCFA. Advance-staged fibroatheromas show more necrotic core volume and more dense calcium than small, early-stage fibroatheromas.

A case of type 3 hyperlipoproteinemia associated with generalized tuberoeruptive xanthomas / 대한내과학회지

A 55-year-old female presented with extensive yellowish eruptive plaques over both elbows and the buttocks that she had first noticed 2 years earlier. Yellowish orange discoloration of her palmar creases was noted. Her serum cholesterol and triglyceride were markedly elevated. Lipoprotein electrophoresis showed a broad beta band. On apolipoprotein E genotyping, the arginine at position 158 had been replaced by cysteine in both alleles (E2/E2). Under a diagnosis of type III hyperlipoproteinemia, combined atorvastatin and fenofibrate therapy for 2 months normalized the serum cholesterol and triglyceride levels.