The Effect of Doubling the Statin Dose on Pro-Inflammatory Cytokine in Patients With Triple-Vessel Coronary Artery Disease

BACKGROUND AND OBJECTIVES: Statin prevents atherosclerotic progression and helps to stabilize the plaque. According to a recent study, statin reduces inflammation in blood vessels. However, it has not been demonstrated to have any anti-inflammation reaction in patients who have been diagnosed as having a triple-vessel coronary artery disease (CAD). SUBJECTS AND METHODS: This study included a total of thirty (30) patients who had been diagnosed by coronary angiogram as having a triple-vessel CAD. Patients who already had been taking statin were given doubled dosage. An interview, physical examination and blood test were performed at the beginning of this study and three months later. RESULTS: After doubling the dose of statin, there was no statistically significant decrease in total cholesterol, low density lipoprotein-cholesterol, (increase in) high density lipoprotein-cholesterol and triglyceride in the blood test. C-reactive protein (CRP), an acute phase reactant, significantly decreased from 0.34 mg/dL at the beginning of the study to 0.12 mg/dL at the end of study (p<0.01). The interleukin-6 concentration also significantly decreased from 8.55 pg/dL to 4.81 pg/dL (p<0.001). No major cardiovascular events occurred and the dosage regimen was not modified during the close observation period. There was no difference in the symptoms of angina pectoris, established by World Health Organization Angina Questionnaires, before and after the dose increase. Liver enzymes remained within normal range with no significant increase before and after conducting this study. CONCLUSION: Doubling the dose of statin alone significantly lowers pro-inflammatory cytokine concentration, which is closely related to the potential acute coronary syndrome, and CRP, a marker of vascular inflammation.

Effect of Lacidipine on Blood Pressure and Endothelial Function in Mild-to-Moderate Essential Hypertension Patients With Diabetes in Korea

BACKGROUND AND OBJECTIVES: The aim of this study was to evaluate the efficacy of lacidipine in reducing blood pressure (BP) and to determine its effect on endothelial function in mild-to-moderate hypertensive patients with type 2 diabetes mellitus (DM). SUBJECTS AND METHODS: This was a prospective, multicenter, open-label, single-arm study, enrolling 290 patients with mild-to-moderate hypertension and type 2 DM. Patients were initially treated with 2 mg lacidipine orally once daily for 4 weeks, which was then increased as necessary every 4 weeks to a maximal dose of 6 mg daily. The primary endpoint was the mean change in systolic blood pressure (SBP) from baseline after 12 weeks of treatment. Secondary endpoints included mean changes in diastolic blood pressure (DBP), flow-mediated vasodilatation (FMD), and serum concentrations of biochemical markers such as high-sensitivity C-reactive protein (hs-CRP), monocyte chemo-attractant protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9), and plasminogen activator inhibitor-1 (PAI-1). RESULTS: Lacidipine treatment significantly reduced SBP by -13.4+/-13.0 mmHg (p<0.001) and DBP by -6.2+/-9.3 mmHg (p<0.001). Lacidipine treatment did not improve endothelial-dependent vasodilatation, despite significantly improved nitroglycerin-induced, endothelial-independent vasodilatation. MCP-1 levels significantly decreased from 283.66+/-110.08 pg/mL to 257.83+/-100.23 pg/mL (p<0.001); whereas there were no significant changes in the levels of hs-CRP, MMP-9, or PAI-1. CONCLUSION: Twelve weeks of treatment with lacidipine was effective and well tolerated in mild-to-moderate hypertensive patients with type 2 DM. In spite of inducing a significant reduction in MCP-1 levels, lacidipine did not improve endothelial function.

Leptin is Associated with Endothelial Dysfunction in Healthy Obese Premenopausal Women

BACKGROUND AND OBJECTIVES: Previous studies have demonstrated that adipokines can have positive and/or negative effects on vascular function. In this study, we attempted to characterize the association of adipokines with endothelium-dependent vasodilation in healthy premenopausal women. SUBJECTS AND METHODS: Noninvasive pulse wave analysis coupled with provocative pharmacological testing with salbutamol was used to measure endothelium-dependent vasodilation in 60 healthy premenopausal women [37 obese women; body mass index (BMI) > or = 25 kg/m2, 23 age-matched non-obese women; BMI<25 kg/m2]. The lipid profile, fasting insulin, glucose, and C-reactive protein (CRP) concentrations in each patient were assessed via standard laboratory techniques, and plasma concentrations of various adipokines, such as adiponectin, leptin, resistin and TNF-alpha, were measured via enzyme immunoassays. RESULTS: In the obese group, higher leptin concentrations were significantly associated with impairments in endothelium-dependent vasodilation (r=-0.371, p=0.005). This association remained significant, even after adjustment for other risk factors (beta=-0.39, p=0.006). However, we determined that there was no significant correlation between endothelium-dependent vasodilation and these variables in the obese group and the control group. CONSLUSION: Increased plasma concentration of leptin was associated with impairment in endothelial function in obese premenopausal women, regardless of the metabolic and inflammatory disturbances associated with obesity.

Risk Factors for Acute Cardioembolic Brain Stroke in Acute Myocardial Infarction

BACKGROUND AND OBJECTIVES: An ischemic brain stroke following acute myocardial infarction (AMI) has a poor clinical prognosis, which primarily results from a thromboembolism. We determined the risk factors of acute cardioembolic brain stroke events that developed concurrently with, or soon after, the onset of AMI. SUBJECTS AND METHODS: We evaluated 38 AMI patients, who developed subsequent acute cardioembolic brain stroke during their index admission, by comparing their clinical and angiographic characteristics with those of 1,443 consecutive patients that had not experienced a brain stroke. Strokes that occurred between the onset of the AMI and patient discharge were analyzed. The incidences of cardiovascular risk factors, and the clinical and angiographic characteristics, of patients admitted to Ewha Womans University Mokdong Hospital, with a diagnosis of AMI over a 10-year period, were compared. RESULTS: In the univariate analysis, the frequencies of atrial fibrillation (21% vs. 4%, p=0.011) and hypertension (71% vs. 48%, p=0.030), and a left ventricular ejection fraction <40% (52% vs. 33%, p=0.039) were significantly higher in patients that had had an acute cardioembolic brain stroke. In a logistical regression analysis, atrial fibrillation was found to be a significant contributor to the subsequent development of an acute cardioembolic brain stroke in the AMI patients (p=0.023, beta=2.025, odds ratio=7.6). Mean follow-up period, which was mainly determined as the time to death after the AMI, was shorter in the acute cardioembolic brain stroke patients (8.5 month vs. 24.3 month, p=0.002). The death rate during the mean follow-up period was much higher in these patients (50% vs. 29%). CONCLUSION: We found that the presence of atrial fibrillation at the time of admission for an AMI was associated with an increased risk of a subsequent acute cardioembolic brain stroke.

Stent Thrombosis after Successful Drug-Eluting Stent Implantation

BACKGROUND AND OBJECTIVES: Stent thrombosis (ST) after a successful drug-eluting stent (DES) implantation has been reported in around 1% of clinical trials. However, the incidence of ST with a DES in practice is not well known. Here, we evaluated the possible causes of ST encountered in four Korean hospitals. SUBJECTS AND METHODS: Between March 2003 and December 2003, 450 patients were treated using a DES in the four study hospitals. We reviewed the clinical and procedural characteristics of 8 patients that experienced ST after a successful DES implantation. RESULTS: Eight patients (1.8%), who were administered antiplatelet medication, experienced ST, with a mortality of 50% at the 2 month follow-up. ST occurred within 7 days in all patients, with the exception of one, with an occurrence 37 days after intervention. Initially, all patients were diagnosed as having acute coronary syndrome. Direct PTCA was performed in 3 patients (38%). Severe calcification or a thrombus was noted in 6 (67%) of 9 lesions. In all cases, no GPIIbIIIa inhibitors were used prior to the DES implantation. Incomplete lesion coverage and incomplete stent expansion appeared in 7 (88%) cases. CONCLUSION: Our study demonstrated that full expansion of the DES and complete lesion coverage must be accomplished, with high pressure inflation or use of cutting balloon preferably under IVUS guidance, for the prevention of ST. Those patients with acute coronary syndrome might warrant intensive antiplatelet therapy, including GPIIbIIIa inhibitors.

Delayed Ventricular Septal Rupture after Percutaneous Coronary Intervention in Acute Myocardial Infarction

In the era before reperfusion therapy, ventricular septal rupture complicated 1~3% of acute myocardial infarctions (AMI) usually 3-5 days after onset. Studies have reported a positive correlation between the incidence of septal perforation and total occlusion of the coronary arteries. A 70-year old female patient was referred to the emergency room with the diagnosis of acute anterior myocardial infarction (MI) and recent cerebral infarction. The coronary angiogram showed a 90% stenosis at the mid-portion of the left anterior descending artery (LAD), and the lesion was successfully treated by percutaneous coronary intervention (PCI) with stent implantation. After PCI, the anterior wall motion improved on the follow-up echocardiogram. However, on the 20th hospital day, the patient condition deteriorated suddenly with pulmonary congestion. The echocardiography revealed a 1.3 cm ventricular septal defect at the apical septum with a left-to-right shunt. We report this rare case of delayed septal rupture in a patient with patent LAD after PCI and recovery of wall motion.

Reduction in Visceral Adiposity is Highly Related to Improvement in Vascular Endothelial Dysfunction among Obese Women: An Assessment of Endothelial Function by Radial Artery Pulse Wave Analysis

Because obesity is frequently complicated by other cardiovascular risk factors, the impact of a reduction in visceral adiposity on vascular endothelial dysfunction (VED) in obese patients is difficult to determine. In the present study, we evaluated the impact of a reduction in visceral adiposity on VED in obese women. Thirty-six premenopausal obese women (BMI > or = 25 kg/m2) without complications were enrolled in the study. VED was evaluated by determining the augmentation index (AIx) from radial artery pulse waves obtained by applanation tonometry. Changes in AIx in response to nitroglycerin- induced endothelium-independent vasodilatation (delta AIx-NTG) and in response to salbutamol administration (delta AIx-Salb) were determined before and after weight reduction. After a 12-week weight reduction program, the average weight loss was 7.96 +/- 3.47 kg, with losses of 21.88 +/- 20.39 cm2 in visceral fat areas (p 0.1) and an improvement in endothelial-dependent vasodilation following weight reduction (delta AIx-Salb: 10.03 +/- 6.49% before weight reduction vs. 19.33 +/- 9.28% after reduction, p < 0.001). A reduction in visceral adipose tissue was found to be most significantly related to an increase in delta AIx-Salb (beta=-0.57, p < 0.001). A reduction in visceral adiposity was significantly related to an improvement in VED. This finding suggests that reduction of visceral adiposity may be as important as the control of other major risk factors in the prevention of atherosclerosis in obese women.

Drug-Eluting Stent Used to Treat a Case of Recurrent Right Coronary Artery In-Stent Restenoses often Accompanied by Acute Inferior Wall Myocardial Infarction

We successfully treated a case of in-stent restenosis, which presented on 6 occasions, resulting in frequent acute inferior wall myocardial infarctions, using a drug-eluting stent. This case demonstrates that drug-eluting stents offer the promise of an effective treatment for frequent in-stent restenosis, and importantly, that the underexpansion of a drug-eluting stent heightens the risk of acute or subacute stent thrombosis.

CT Coronary Angiography Using Multidetector Computed Tomography in Coronary Artery Disease : A Comparative Study to Quantitative Coronary Angiography

BACKGROUND AND OBJECTIVES: The purpose of the present study was to investigate the diagnostic accuracy of coronary stenoses in patients with ischemic heart disease using multidetector CT coronary angiography (MDCT) in the assessment of coronary artery disease. SUBJECTS AND METHODS: Forty-three patients (49-72yrs) undergoing conventional coronary angiography (CCA) were included in this study. All patients were premedicated with oral propranolol, 40-80 mg, to achieve an acceptable heart rate of less than 65 bpm, 1hr before the MDCT. All coronary arteries, including the distal segments and side branches, were assessed with respect to assessability and the presence of significant stenosis (>50%) and the results compared with those of CCA. RESULTS: Of the 645 coronary artery segments scanned, 540 were assessable (84%). A total 44 significant stenoses were detected by CCA and 49 lesions by MDCT. The overall sensitivity and specificity were 77 and 97%, respectively. The overall accuracy for the LAD, RCA and LCX was 94, 98 and 95%, respectively, and there were no differences in the accuracies in each vessel. The sensitivity in the proximal segments was much higher than in the distal segments. A total 15 segments were overestimated by the MDCT due to calcification and the small vessel size. CONCLUSION: MDCT, with improved spatial and temporal resolutions, and pre-treated with oral beta-blocker, permits the detection of coronary artery stenoses with a high degree of accuracy.

A Case of Native Valve Salvage for 8 Years Longstanding Ruptured Tricuspid Valve after Blunt Chest Trauma

Although very rare, the incidence of tricuspid valve regurgitation after blunt chest trauma has risen in line with the increasing rate of car accidents and steering wheel trauma. It is easy to miss the diagnosis of tricuspid valve regurgitation following blunt chest trauma because most patients feel no symptoms at trauma, and the condition is sometimes overlooked for a long period of time due to its mild symptoms. A 49-year-old man suffered dyspnea on exertion for 1 month due to right heart failure 8 years after accidentally falling from a third floor. Preoperative echocardiography revealed severe tricuspid valve regurgitation resulting from prolapse of the anterior leaflet with annular dilatation. The patient underwent tricuspid valvuloplasty with a 36-mm Carpentier tricuspid ring. Intraoperative transesophageal echocardiography showed mild tricuspid valve regurgitation. We report a case of successful native valve salvage of ruptured tricuspid valve after blunt chest trauma, and present a review of the relevant literature.

A Case of Native Valve Salvage for 8 Years Longstanding Ruptured Tricuspid Valve after Blunt Chest Trauma

Although very rare, the incidence of tricuspid valve regurgitation after blunt chest trauma has risen in line with the increasing rate of car accidents and steering wheel trauma. It is easy to miss the diagnosis of tricuspid valve regurgitation following blunt chest trauma because most patients feel no symptoms at trauma, and the condition is sometimes overlooked for a long period of time due to its mild symptoms. A 49-year-old man suffered dyspnea on exertion for 1 month due to right heart failure 8 years after accidentally falling from a third floor. Preoperative echocardiography revealed severe tricuspid valve regurgitation resulting from prolapse of the anterior leaflet with annular dilatation. The patient underwent tricuspid valvuloplasty with a 36-mm Carpentier tricuspid ring. Intraoperative transesophageal echocardiography showed mild tricuspid valve regurgitation. We report a case of successful native valve salvage of ruptured tricuspid valve after blunt chest trauma, and present a review of the relevant literature.

A Case of Myocardial Stunning in Hyperthyroidism

Although myocardial stunning occurs in coronary artery disease, it has rarely been reported with hyperthyroidism. A 72-year-old woman presented with general weakness, shortness of breath and febrile sensation of 10 days duration. The serum thyroid hormone level was elevated. Serial EKGs showed significant ST elevation suggesting transmural ischemia, but coronary angiography was not significant. Echocardiography showed regional wall motion abnormality of apical hypokinesia, which was improved after medication for hyperthyroidism. We report this case as an example of myocardial stunning associated with hyperthyroidism.

A Case of Myocardial Stunning in Hyperthyroidism

Although myocardial stunning occurs in coronary artery disease, it has rarely been reported with hyperthyroidism. A 72-year-old woman presented with general weakness, shortness of breath and febrile sensation of 10 days duration. The serum thyroid hormone level was elevated. Serial EKGs showed significant ST elevation suggesting transmural ischemia, but coronary angiography was not significant. Echocardiography showed regional wall motion abnormality of apical hypokinesia, which was improved after medication for hyperthyroidism. We report this case as an example of myocardial stunning associated with hyperthyroidism.

Two Cases of Haemophilus parainfluenzae endocarditis / 감염과화학요법

HACEK organisms are the normal flora of upper respiratory tract and orophaynx. They infect abnormal cardiac valves, causing subacute native valve endocarditis or prosthetic valve endocarditis more than one year after valve surgery. Haemophilus species are responsible for only 0.5-1% of all infectious endocarditis cases. Embolization occurs in 60% and the mortality rate ranges from 16-45% of cases of infective endocarditis caused by H. parainfluenzae. We report two cases of H. parainfluenzae endocarditis, one of them is a 25-year-old male with tricuspid valve vegetations complicated with pulmonary embolism and the other is a 22-year-old female presented with heart failure.

Two Cases of Haemophilus parainfluenzae endocarditis / 감염과화학요법

HACEK organisms are the normal flora of upper respiratory tract and orophaynx. They infect abnormal cardiac valves, causing subacute native valve endocarditis or prosthetic valve endocarditis more than one year after valve surgery. Haemophilus species are responsible for only 0.5-1% of all infectious endocarditis cases. Embolization occurs in 60% and the mortality rate ranges from 16-45% of cases of infective endocarditis caused by H. parainfluenzae. We report two cases of H. parainfluenzae endocarditis, one of them is a 25-year-old male with tricuspid valve vegetations complicated with pulmonary embolism and the other is a 22-year-old female presented with heart failure.

Relationship of Adiponectin to Body fat Distribution, Insulin Sensitivity and Plasma Lipoproteins: in Healthy Premenopausal Women

BACKGROUND AND OBJECTIVES: The precise mechanism linking obesity and vascular disease is still unclear. Previous studies have demonstrated that the plasma levels of adiponectin, an adipose-derived hormone, decrease in obese subjects, and that hypoadiponectinemia are associated with ischemic heart disease. In this study, we investigated the determinant factors of plasma adiponectin concentration in healthy premenopausal women. SUBJECTS AND METHODS: We analyzed the plasma adiponectin concentrations in healthy, obese premenopausal women (n=37, BMI> or =25 Kg/m2) and in age-matched, healthy, non-obese premenopausal women (n=23, BMI<25 Kg/m2). The visceral and subcutaneous fat areas were measured by CT scan. RESULTS: Plasma levels of adiponectin in the obese subjects were lower than those in the non-obese subjects (3.24+/-1.08 vs. 4.90+/-2.06 microgram/ml, p<0.01). Significant, univariate, inverse correlations were observed between plasma adiponectin levels and visceral fat areas (r=-0.643, p<0.001), and between adiponectin levels and subcutaneous fat areas (r=-0.407, p<0.01). In univariate analysis, adiponectin was directly related to insulin sensitivity, hsCRP, triglyceride, HDL and LDL cholesterol. In multivariate analysis, visceral fat areas (beta=-0.483, p=0.001) and HDL cholesterol remained significantly related to plasma adiponectin concentrations (beta=0.283, p<0.05). CONCLUSION: These results suggest that HDL cholesterol and visceral fat mass were independently associated with plasma concentrations of adiponectin.

Dose Dependent Changes of Lipid Profiles, IL-6 and CRP in Unstable Angina Patients after Simvastatin Therapy

BACKGROUND AND OBJECTIVES: The beneficial effects of statins in preventing cardiovascular events may depend, in part, on their anti-inflammatory action. We previously reported that low dose statin therapy has cholesterol lowering effects, but no effect on inflammation, and proposed that a sufficient dose of therapy might be needed to achieve anti-inflammatory action. The aims of this study were to confirm the suggestions made in our previous study. SUBJECTS AND METHODS: Fifteen unstable angina patients who were enrolled in our previous study were evaluated. The usual dose (20 mg) of simvastatin was administrated for 26 weeks, blood samples collected following the administration and tested for their lipid profiles and inflammatory markers (IL-6, CRP). The changes in the lipid profiles and inflammatory markers, from baseline levels, to the usual and low doses of statin therapy were evaluated. RESULTS: The changes in the IL-6 and hsCRP levels after the usual dose simvastatin therapy compared with the baseline levels were -72.8 and -59.6% (p< 0.05), respectively. The changes in the IL-6 and hsCRP levels after the usual dose simvastatin therapy compared with a 5 mg dose were -77.2 and -47.1% (p< 0.05), respectively. There was statistically significant correlation between the change in the levels of IL-6 and hsCRP during statin therapy. CONCLUSION: Our data confirmed the preliminary result of Chung et al, which suggested the usual dose of simvastatin is required to inhibit the inflammation of unstable plaque in patients with unstable angina associated with hypercholesterolemia.

Percutaneous Coronary Intervention

Since the introduction of percutaneous balloon angioplasty by Gruentzig in 1979, percutaneous coronary intervention (PCI) has become the main treatment modality for the management of coronary heart disease. More than 1,000,000 PCI procedures are performed annually worldwide. With the advent of new therapeutic technologies, the indications for PCI have markedly expanded. Nowadays, improvements in balloon technology, popular use of coronary stent, and the proper administration of antiplatelet agents including GPIIbIIIa inhibitors have influenced the acute procedural outcomes. This technological and procedural advance in PCI has resulted in angiographic success rates of 96 to 99%, with Q-wave MI rates of 1 to 3%, emergency coronary bypass surgery rates of 0.2 to 3%, and unadjusted in-hospital mortality rates of 0.5~1.4%. However, despite the marked improvements in the acute outcome of PCI, long-term results including the restenosis rate are less impressive. The restenosis rate following balloon angioplasty reaches 30~40%, and is higher in certain clinical and angiographic subsets. The recent introduction of intracoronary stent and brachytherapy (intracoronary lesional ionizing radiation therapy) has a favorable impact on the restenosis precess including elastic recoil and intimal hyperplasia. Intracoronary stents decreased elastic recoil and remodeling and intracoronary radiation reduced intimal hyperplasia. Several randomized clinical trials to assess the efficacy of stents and intracoronary brachytherapy are ongoing with impressive results. In 2001, a breakthrough has been made in the prevention and the treatment of restenosis with the advent of a drug-eluting stent. Balloon-expandable stents coated with rapamycin or paclitaxol showed nearly 0% restenosis rate at 6-month follow-up. We might expect to solve restenosis completely in a very near future.

The Change of Cholesterol Level and IL-6, CRP in Unstable Angina Patients with Hypercholesterolemia after Low Dose Simvastatin Therapy

BACKGROUND AND OBJECTIVES: Cardiovascular mortality in patients with atherosclerosis can be reduced by treatment with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors. This proven effect is probably due, not only to the cholesterol lowering effect, but also to the non-lipid-lowering mechanisms elicited by the action of statins. These results, however, were achieved with high or usual doses of statin therapy, whereas similar results with low dose statins are rare. The aims of this study wereas to investigate the changes ofin cholesterol level and the inflammatory markers, Interleukin-6(IL-6), and C-Reactive protein (CRP), in unstable angina patients with hypercholesterolemia, using low dose simvastatin therapy. SUBJECTS AND METHODS: Eighteen unstable angina patients (55+/-6 years, M : F=10 : 8, Baunwald class IIIb) with hypercholesterolemia (a LDL -cholesterol level over 100 mg/dL) were evaluated. A Llow dose of simvastatin (5 mg) was administrated for 4 weeks. The changes of total cholesterol, LDL-cholesterol, triglyceride, HDL-cholesterol and the inflammatory markers, IL-6, and CRP, were all elevated from the baseline following 4 weeks of treatment. RESULTS: The baseline mean values of total cholesterol, LDL-cholesterol, triglyceride, and HDL-cholesterol were 237.1+/-56.9 mg/dL, 131.9+/-39.0 mg/dL, 168.3+/-20.4 mg/dL, and 50.0+/-3.8 mg/dL, respectively. The baseline mean values of IL-6 and hs CRP were 6.842+/-6.661 pg/mL, and 0.866+/-1.083 mg/dL, respectively. Following the 4 weeks of simvastatin treatment, the levels of total cholesterol, LDL- cholesterol, triglyceride, and HDL-cholesterol were 200.8+/-47.5 mg/dL, 101.6+/-35.4 mg/dlL, 155.8+/-18.6 mg/dL, and 47.0+/-2.3 mg/dL, respectively, giving percentage changes of -17.6% (p0.05), and -2.1% (p>0.05), respectively. Following the 4 weeks of treatment, the levels of IL-6 and hs CRP were 6.955+/-5.555 pg/mL, and 0.753+/-0.571 mg/dL, respectively, giving percentage changes of 51.8 (p>0.05), and 36.5% (p>0.05), respectively. There was no significant correlation between the level of LDL-cholesterol and the levels of IL-6, or hs CRP at the baseline, or post-treatment. There was also no significant correlation between the change of LDL-cholesterol and the changes of IL-6 or hs CRP levels during the simvastatin therapy. There was no significant correlation between the levels of IL-6 and hs CRP at the baseline or ost-treatment. CONCLUSION: Our data showed that in patients with unstable angina patients with coupled with hypercholesterolemia, low dose statin therapy has a cholesterol lowering effect, but no effect on inflammation.

A Case of Severe Hypokalemia Induced by Chronic Furosemide Abuse / 대한신장학회잡지

A 46-year-old woman was admitted to emergency room for muscle weakness and repiratory difficulty. She was taking furosemide (4 tablets per day : 160 mg/day) without physician's prescription. Her blood pressure was 90/50 mmHg and her heart rate 74/ min. Her laboratory finding showed a low serum potassium concentration (0.9 mmol/L), CK 368 IU/L, creatine 1.6 mg/dL. The result was rechecked and confirmed. Electrocardiography showed a dip in the ST segment, prolonged QTc, 1st degree AV block and 2 : 1 AV block. Echocardiography was normal. Abdominal CT scan show right lower pole calyceal stones without nephrocalcinosis. Treatment was initiated consisting of intravenous potassium chloride. Hypokalemia was overcome in 3 days. Kidney biopsy showed hypokalemic nephropathy - interstitial nephrosis, vacuolar change of tubule, proliferation of juxtaglomerular apparatus. Paralytic ileus, rebound pleural effusion, glucose intolerance, elevation of CK were associated findings. After correction of hypokalemia, her symptoms and electrocardiographic findings returned to normal.