Proteinuria / 대한내과학회지

No abstract available.

Exertional heat stroke: clinical characteristics and courses of 15 patients / 대한내과학회지

BACKGROUND: Heat stroke is a life-threatening emergency and manifested principally by hyperthermia and central nervous system dysfunction. Exertional heat stroke seems to be more predominant type in Korea, considering its temperate climate. We undertook this study to evaluate the clinical characteristics and courses of exertional heat stroke. METHODS: Serial clinical and laboratory data were collected and analyzed in 15 patients with exertional heat stroke from April 2000 to October 2001. RESULTS: Most episodes occurred after heavy exercise during periods of high ambient temperature and humidity. Especially 11 patients (73.3%) were unacclimatized recruits in basic training. Victims showed a characteristic clinical feature such as high core body temperature (>40degrees C), altered mental status and frequent shock (7 cases). Common abnormal laboratory findings were: elevated serum CPK, LDH, AST and myoglobin, elevated ALT, leukocytosis, thrombocytopenia, metabolic acidosis and typical electrocardiographic abnormalities. All patients presented with normal or hypokalemic state (50%), although they were complicated with renal failure, rhabdomyolysis and metabolic acidosis. Heat stoke induced multiple organ failure such as rhabdomyolysis (93.3%), acute renal failure (73.3%), disseminated intravascular coagulation (46.7%), myocardial ischemia (28.6%) in addition to central nervous system dysfunction. Three patients (20%) died and 3 patients among survivors suffered from persisting CNS dysfunction, especially cerebellar dysfunction. CONCLUSION: Heat stroke is a fatal emergency with high mortality and morbidity. Heat stroke should be suspected in any person who collapses during physical activity, especially on a hot and humid day and the prompt initiation of appropriate treatment is demanded.

A Case of Clomipramine-Induced Chronic Dilated Cardiomyopathy

Dilated cardiomyopathy is a primary myocardial disease characterized by ventricular dilatation and impaired ventricular contractility. The etiology of dilated cardiomyopathy has not been known yet, but toxin such as alcohol, thiamine deficiency, endocrine disorder, viral or bacterial infection, hereditary disorder, and muscular dystrophy may be related to dilated cardiomyopathy. Cocaine abuse and anticancer drugs (especially doxorubicin) were reported as the causes of drugs of dilated cardiomyopathy also. Recently we experinced a case of dilated cardiomyopathy in 30 years old man who developed dilated cardiomyopathy on chronic clomipramine (one of trcyclic antidepressant drugs) treatment for a obsessive-compulsive disorder. He became asymptomatic and normalization of left ventricular diameters and function was evidenced echocardiographically after withdrawal of the drug. The possible association of cardiomyopathy and tricyclic antidepressant drugs and possibility of functional improvement after tricyclic antidepressant drugs withdrawal should be kept in mind.

Effect of Diltiazem on Myocardial and Microvascular Stunning in Open Chest Dog

BACKGROUND: Post-ischemic myocardial dysfunction (myocardial stunning) is known to be associated with low reflow phenomenon or the reduction of coronary vasodilatory reserve. However, it remains controversial whether a relationship between myocardial stunning and post-ischemic impairment of coronary flow reserve exists. With increased influx of calcium into myocardial cells precipitated by ischemia and reperfusion known to be involved not only in the progression of myocardial tissue damage but also in the pathogenesis of post-ischemic myocardial dysfunction and impaired coronary vasodilatory reserve, it has been hypothesized that calcium channel blockers exert protective effects on post-ischemic myocardial dysfunction and microvascular dysfunction. PURPOSE: To investigate the effects of diltiazem, a calcium channel blocker, on post-ischemic myocardial dysfunction and coronary vasodilatory reserve, vehicle or diltiazem was administered before brief coronary artery occlusion in open chest dogs. Peak coronary flow and myocardial contractile function were measured after intracoronary infusion of endothelium-dependent vasodilator acetylcholine and endothelium-independent vasodilator adenosine. The parameters measured before and after reperfusion in control dogs and diltiazem-treated dogs were compared. METHOD: Open chest dogs (n-17) underwent 20 minutes occlusion of left circumflex artery followed by reperfusion for 60 minutes:the subjects were divided into two groups (n-10 in control group and n-7 in diltiazem group). Diltiazem dogs received diltiazem (0.2 mg/kg) intravenuously 15 minutes before coronary occlusion. Control dogs received vehicle-a saline solution. Coronary blood flow was measured with electromagnetic flow probe. Coronary flow reserve was determined by peak coronary flow after intracoronary infusion of acetylcholine (ACH, 0.01ug/kg) and adenosine (ADE, 1.5 mg/kg):it was also determined by reactive hyperemia (RH) measured after coronary occlusion for 20 seconds at baseline and 30 and 60 minutes after reperfusion. Segmental left ventricular function was assessed by 2-D echocardiography at the level of mid-papillary muscle, and changes of left ventricular function was expressed as % change of myocardial thickening and % change of endocardial thickening. RESULTS: Peak coronary flow and minimal coronary vascular resistance with ACH, ADE and RH were maintained at 30 and 60 minutes after reperfusion in the diltiazem group, but those in the control group were significantly impaired. There was no difference in reduction of % change of peak flow with ACH in both groups (p-0.44), but the reduction of % change of peak flow with ADE was attenuated in the diltiazem group when compared with the control group (p-0.03) 60 minutes after reperfusion. Total myocardial thickening and endocardial wall motion at 30 and 60 minutes after reperfusion were significantly reduced than those assessed before coronary occlusion in both groups, but the endocardial wall motion was less depressed in the diltiazem group than that in the control group. There was no correlation between % change of peak flow in response to ACH and to ADE and % change of myocardial thickening:there was also no correlation between % change of endocardial wall motion in the control group and % change of myocardial thickening in the diltiazem group. There was however good correlation between % change of peak flow and % change of endocardial wall motion in the diltiazem group. CONCLUSION: The findings that changes in peak coronary flow and minimal coronary vascular resistance do not correlate with the change in myocardial contractile function in the dog model with reperfusion after 20 minutes coronary occlusion suggest that microvascular and myocardial stunning develop independent of each other. The protective effect of diltiazem on impaired coronary flow reserve and contractile dysfunction following reperfusion after brief ischemia also suggests that calcium overloading plays a role in the pathogenesis of microvascular stunning as well as myocardial stunning.

Relation between Perfusion Status of Dysfunctional Myocardium and Coronary Flow Reserve in Acute Myocardial Infarction

BACKGROUND: Dydfunction of microvasculature was frequently observed despite of successful revascularization with alteration of coronary flow dynamics flow dynamics in acute myocardial infarction (AMI). Reduction of coronary vasodilatory reserve was found in poorly perfused infarcted myocardium. The objectives of this study was to evaluate the vasodilatory reserve in infarcted myocardium and determind its relationship to perfusion status of myocardium in early recovery phase of acute myocardial infarction. METHODS: The study subjects consisted of 14 patients with anterior AMI&and 6 controls with atypical chest pain and have normal coronary artery. The coronary flow pattern was assessed using intracoronary Doppler wire and vasodilatory reserve was measured after injection of 18ug of adenosine to infarct-related artery after successful revascularization by percutaneous angioplasty at average 11 days post-AMI After measurement of coronary blood flow pattern, myocardial perfusion status was evaluated by myocardial contrast echocardiography (MCE). Perfusion status by MCE was analysed semiquantitatively and compared to various parameters of coronary flow and vasodilatory reserve of infarct-related artery. RESULTS: After successful revascularization, perfusion defect by MCE was observed in 50% (n=7) of patients. The vasodilatory reserve was lower in patients with perfusion defect by MCE than those of patients without perfusion defect (p<0.05) and control (p<0.05). There was no difference in coronary flow reserve between patients with no perfusion defect and controls (p=0.54). Coronary flow reserve was more than 2.0 in patients with no perfusion defect and was below 2.0 in patients with perfusion defect except one patients. Coronary flow reserve correlated well with the degree of contrast opacification of left anterior descending artery territory (r=0.80, p=0.005). The increments of peak distolic velocity (r=0.63, p=0.016 vs r=0.3, p=0.29). CONCLUSIONS: These data showed a good correlation of coronary flow reserve with the degree of myocardial perfusion in patients of reperfused acute myocardial infarction. The increments of peak diastolic velocity was important to maintain the coronary flow than that of systolic peak velocity. This suggest that the measurement of vasodilatory reserve by intracoronary Doppler wire is a good method to assess the perfusion status of infarcted myocardium in early recovery phase of AMI.

Effects of Ischemic preconditioning on the Post-ischemic Myocardial Dysfunction and Coronary Flow in the Isolated Rat Hearts

BACKGROUND: Brief episodic ischemias prior to subsequent prolonged ischemia limit infarct size and attenuate the reperfusion arrythmia. But the effect of ischemic preconditioning on post-ischemic myocardial dysfunction, coronary flow and nitric oxide (NO) remains unclear. METHODS: To investigate the effect of ischemic preconditioning on myocardial function and coronary flow during reperfusion after 15 minutes of global myocardial ischemia, 30 isolated hearts of Sprague-Dowley rats were perfused under constant pressure. Two episodes of three minutes global ischemia followed by 12 minutes of reflow were employed to precondition the hearts. The hearts were randomized to one of three groups : group I had no preconditioning, group II had preconditioning, group III had preconditioning as well as L-arginine pretreatment. Left ventricular developed pressure (LVDP), LV dp/dt, perfused coronary flow, concentration of NO and heart rate were continuously measured. RESULTS: In preconditioning groups (Group II, Group III), LVDP decreased during reflow and was lower than that of the control group. LV dp/dt decreased after reflow and gradually recovered with time but recovered was less in preconditioning groups. Coronary flow increased in the first few minutes after reflow in all groups, but decreased gradually. The decrease of coronary flow was greater in preconditioning groups. NO increased during the first 10 minutes after reflow and then decreased. In preconditioning groups, NO tends to be lower than that in the non-preconditioning group. CONCLUSION: Ischemic preconditioning was not beneficial to post-ischemic myocardial dysfunction, coronary flow and NO concentration in the flow. Cummulative effect of stunning due to repetitive ischemia for preconditioning may be an explanation for worse post-ischemic myocardial dysfunction and coronary flow in preconditioning groups.

Effects of Ischemic preconditioning on the Post-ischemic Myocardial Dysfunction and Coronary Flow in the Isolated Rat Hearts

BACKGROUND: Brief episodic ischemias prior to subsequent prolonged ischemia limit infarct size and attenuate the reperfusion arrythmia. But the effect of ischemic preconditioning on post-ischemic myocardial dysfunction, coronary flow and nitric oxide (NO) remains unclear. METHODS: To investigate the effect of ischemic preconditioning on myocardial function and coronary flow during reperfusion after 15 minutes of global myocardial ischemia, 30 isolated hearts of Sprague-Dowley rats were perfused under constant pressure. Two episodes of three minutes global ischemia followed by 12 minutes of reflow were employed to precondition the hearts. The hearts were randomized to one of three groups : group I had no preconditioning, group II had preconditioning, group III had preconditioning as well as L-arginine pretreatment. Left ventricular developed pressure (LVDP), LV dp/dt, perfused coronary flow, concentration of NO and heart rate were continuously measured. RESULTS: In preconditioning groups (Group II, Group III), LVDP decreased during reflow and was lower than that of the control group. LV dp/dt decreased after reflow and gradually recovered with time but recovered was less in preconditioning groups. Coronary flow increased in the first few minutes after reflow in all groups, but decreased gradually. The decrease of coronary flow was greater in preconditioning groups. NO increased during the first 10 minutes after reflow and then decreased. In preconditioning groups, NO tends to be lower than that in the non-preconditioning group. CONCLUSION: Ischemic preconditioning was not beneficial to post-ischemic myocardial dysfunction, coronary flow and NO concentration in the flow. Cummulative effect of stunning due to repetitive ischemia for preconditioning may be an explanation for worse post-ischemic myocardial dysfunction and coronary flow in preconditioning groups.

Optimal Balloon Inflation Pressures for Stent Deployment: High Pressure is Always Good?

BACKGROUND AND OBJECTIVES: To reduce the subacute stent thrombosis, the use of high pressure final balloon dilatations and confirmation of adequate stent expansion by intravascular ultrasound has been recommended. The purpose of this study is to compare incidence of stent thrombosis and major cardiac events (MACE) between high and moderate pressure balloon technique without using intravascular ultrasound (IVUS) guidance. MATERIALS AND METHODS: We prospectively studied 147 patients (110 males & 37 females, mean;56.9+/-9.9 years, 154 lesions) who were deployed intracoronary stents with the use of conventional technique except IVUS guidance. According to inflation pressure, patients were divided into two groups; G1 (moderate pressure group, maximum inflation balloon pressure or =14ATM, 77 lesions). We investigated the incidence of stent thrombosis and MACE between two groups during the 10 month follow up examination. RESULTS: 1) The mean inflation presure is different between two groups by definition (G1:G2 10.2+/-1.8; 15.2+/-1.3 ATM p<0.001). 2) The stenotic lesion lengths of the group of patients treated with the moderate pressure techique were longer than those treated under the high pressure technique (G1:G2 19.8+/-7.1 mm; 16.3+/-4.1 mm p=0.002). 3) There were no significant differences between the moderate pressure group and the high pressure group during the 10 month follow-up examination in terms of MACE[early event (0-14D)-subacute thrombosis G1:G2 0:0 death G1; G2 1:1/late events (15D - 10M)-repeat revascularization:G1; G2 8; 7, CABG G1; G2 1; 0, Q.M.I G1; G2 1; 0]. CONCLUSION: Onselectedpatients,itispossibletoconsidermoderatepressure technique as an other option for coronary stenting.

Assessment of myocardial perfusion status through the angiographically visible collaterals in the ischemic heart disease

BACKGROUND: It is well known that collateral circulation has important roles in ischemic heart diseases. The method most commonly used at present to evaluate collateral flow is coronary angiography. However, there are debates about the functional significance of angiographically visible collaterals because angiography visualizes only vessels that are larger than 100um in diameter. Recent studies suggest that myocardial contrast echocardiography (MCE) is a useful method in assessing collateral flow because it uses small microvascular tracers (4-12um) as a contrast agent. By using MCE, this study evaluates the role of angiographically visible collaterals in patients with acute myocardial infarction (AMI) and chronic ischemic heart disease. METHOD: Forty-one patients who underwent coronary angiography and MCE were included in this study (22 patients with acute myocardial infarction and 19 patients with chronic ischemic heart disease). Antegrade coronary flow was less than TIMI 3 flow in all patients. Myocardial perfusion through collaterals with MCE was evaluated by injecting sonicated Hexabrix into nonobstructing coronary arteries. Angiographically visualized collateral vessels were analysed as four grades and compared with the degree of myocardial opacification by MCE through collateral vessels. RESULT: Angiographic collaterals were frequently observed in patients with AMI and chronic ischemic heart disease with0.05). CONCLUSION: The study suggests that the role of angiographically visible collaterals is different in chronic ischemic heart disease and acute myocardial infarction. The grade of angiographically visible collaterals does not imply the extent of perfusion to myocardum at risk through collateral vessels.

Relation between Perfusion of Infarcted Myocardium and Exercise-induced ST Shift in Acute Myocardial Infarction

BACKGROUND: It has been demonstrated that within 2 weeks following acute myocardial infarction (AMI), exercise-induced ST-segment depression (STD) indicates subendocardial ischemia in the viable myocardium within infarcted or remote area from the infarction. Exercise-induced ST-segment elevation (STE) in leads with abnormal Q wave is associated with left ventricular dysfunction or aneurysm rather than transmural ischemia. We studied whether each pattern of ST-segment shift on exercise ECG during recovery phase following AMI is correlated with the perfusion status of infarcted myocardium evaluated by myocardial contrast echocardiog-raphy (MCE), regardless of findings of coronary angiography (CAG). METHOD: Study population was consisted of 25 patients with AMI (anteior wall: 11 patients, inferior wall: 14 patients, mean age=57.3+/-8.9years). Patients underwent exercise ECG and coronary angiography at 10 days post-AMI. After CAG, sonicated Hexabrix was injected into both coronory arteries alternatively and 2-D echocardiography was taken in parasternal short axis, apical 4, and 2 chamber views. To analyze the echocardiographic image semiquantitively, left ventricle was divided into 20 segments and perfusion status was graded as good, partial, and no opacification. RESULT: All patients with exercise-induced STE (n=8) in Q-leads had patent infarcted-related artery and poor collaterals on CAG, which was associated with poor or no opacification of infarcted myocardium on MCE. Patients with exercise-induced STD (n=9) frequently had closed infarct-related artery (67%), but good opacification of infarcted myocardium was shown by retrograde perfusion via collaterals, which was commonly seen in patients with multivessel disease. CONCLUSION: In early recovery phase of acute myocardial infarction, exercise-induced ST elevation in Q leads was associated with poor perfusional status in infarcted myocardium, even with patent infarct-related artery on CAG, while exercise-induced ST depression was frequently seen in the good perfusional status despite of closed infarted-related artery, which was commonly observed in patients with multivessel disease.

Relation between Perfusion of Infarcted Myocardium and Exercise-induced ST Shift in Acute Myocardial Infarction

BACKGROUND: It has been demonstrated that within 2 weeks following acute myocardial infarction (AMI), exercise-induced ST-segment depression (STD) indicates subendocardial ischemia in the viable myocardium within infarcted or remote area from the infarction. Exercise-induced ST-segment elevation (STE) in leads with abnormal Q wave is associated with left ventricular dysfunction or aneurysm rather than transmural ischemia. We studied whether each pattern of ST-segment shift on exercise ECG during recovery phase following AMI is correlated with the perfusion status of infarcted myocardium evaluated by myocardial contrast echocardiog-raphy (MCE), regardless of findings of coronary angiography (CAG). METHOD: Study population was consisted of 25 patients with AMI (anteior wall: 11 patients, inferior wall: 14 patients, mean age=57.3+/-8.9years). Patients underwent exercise ECG and coronary angiography at 10 days post-AMI. After CAG, sonicated Hexabrix was injected into both coronory arteries alternatively and 2-D echocardiography was taken in parasternal short axis, apical 4, and 2 chamber views. To analyze the echocardiographic image semiquantitively, left ventricle was divided into 20 segments and perfusion status was graded as good, partial, and no opacification. RESULT: All patients with exercise-induced STE (n=8) in Q-leads had patent infarcted-related artery and poor collaterals on CAG, which was associated with poor or no opacification of infarcted myocardium on MCE. Patients with exercise-induced STD (n=9) frequently had closed infarct-related artery (67%), but good opacification of infarcted myocardium was shown by retrograde perfusion via collaterals, which was commonly seen in patients with multivessel disease. CONCLUSION: In early recovery phase of acute myocardial infarction, exercise-induced ST elevation in Q leads was associated with poor perfusional status in infarcted myocardium, even with patent infarct-related artery on CAG, while exercise-induced ST depression was frequently seen in the good perfusional status despite of closed infarted-related artery, which was commonly observed in patients with multivessel disease.