Carotid stenting and bivalirudin with and without vascular closure: 3-year analysis of procedural outcomes.

OBJECTIVES: The purpose of this study was to examine the outcome of carotid stenting using bivalirudin and the influence of vascular closure devices (VCD) on the incidence and severity of peri-procedural hypotension. BACKGROUND: Bivalirudin, a short-acting direct thrombin inhibitor, has been shown to be an effective anticoagulant in coronary interventions, with less risk of bleeding compared with heparin. Routine use of VCD has become the standard of care, facilitating patient ambulation after percutaneous carotid and coronary interventions. The combined use of these two therapies (bivalirudin and VCD) may improve outcomes in carotid interventions where prolonged patient immobilization may exacerbate hypotension following stenting. METHODS: A total of 514 patients underwent 536 carotid stenting procedures in the 3-year period from September 2004 to September 2007. All patients received adjunctive bivalirudin, with and without VCD. This cohort was analyzed for peri-procedural and 30-day clinical outcomes and length of hospitalization. RESULTS: Thirty-day stroke and death rate was 1.7%. A total of 83 patients (15.4%) experienced intra- or post-procedural hypotension (systolic BP < 80 mm Hg). There were four (0.7%) major bleeding complications requiring transfusion, and length of stay was delayed more than 24 hr in five patients (0.93%), all of whom were in the manual compression group. CONCLUSIONS: This was a negative study, with no significant difference on prolonged hypotensive events in patients with vascular closure device and bivalirudin, compared with those with manual compression and bivalirudin. Vascular closure devices were safe and effective with a low incidence of complications. In carotid artery stenting, bivalirudin is safe with low incidence of major bleeding and acceptable 30-day adverse event rates (stroke and death).

Stent gap by 64-detector computed tomographic angiography relationship to in-stent restenosis, fracture, and overlap failure.

OBJECTIVES: The goal of this study was to define the frequency of stent gaps by 64-detector computed tomographic angiography (CTA) and their relation to in-stent restenosis (ISR), stent fracture (SF), and overlap failure (OF). BACKGROUND: SF defined by catheter angiography or intravascular ultrasound has been implicated in ISR. METHODS: A total of 292 consecutive patients, with 613 stents, who underwent CTA were evaluated for stent gaps associated with decreased Hounsfield units. Correlations with catheter coronary angiography (CCA) were available in 143 patients with 384 stents. RESULTS: Stent gaps were noted in 16.9% by CTA and 1.0% by CCA. ISR by CCA was noted in 46.1% of the stent gaps (p < 0.001) as determined by CCA, and stent gaps by CTA accounted for 27.8% of the total ISR (p < 0.001). In univariate analysis, stent diameter > or =3 mm was the only CCA characteristic significantly associated with stent gaps (p = 0.002), but was not a significant predictor by multivariate analysis. Bifurcation stents, underlying calcification, stent type, location, post-dilation, and overlapping stents were not observed to be predisposing factors. Excessive tortuosity and lack of conformability were not associated with stent gaps; however, their frequency was insufficient to permit meaningful analysis. CONCLUSIONS: Stent gap by CTA: 1) is associated with 28% of ISR, and ISR is found in 46% of stent gaps; 2) is associated with > or =3-mm stents by univariate (p = 0.002) but not by multivariate analysis; 3) is infrequently noted on catheter angiography; and 4) most likely represents SF in the setting of a single stent, and may represent SF or OF in overlapping stents.

Coronary artery disease risk factors in patients with diastolic dysfunction.

Diastolic dysfunction (DD) is a common entity associated with advanced age and hypertension, often present in patients with ischemic heart disease. The correlation of DD and coronary artery disease (CAD) in asymptomatic young patients is not known. We sought to determine the prevalence of CAD risk factors in asymptomatic patients with DD. We present data from a retrospective chart review of CAD risk factors in asymptomatic patients diagnosed with DD during an echocardiograph examination. We screened all patients that had an echocardiographic examination at Lenox Hill Hospital from January 2004 until July 2007. DD was diagnosed if an impaired filling pattern with an E/A ratio less than one was noted on the mitral inflow pulse wave doppler. One-hundred and one patients met study criteria. Data regarding the presence of the following risk factors was collected: sex, hypertension, hyperlipidemia, smoking, diabetes, peripheral artery disease, and family history of CAD. The mean age of patients was 48 +/- 6; 50% were male. The most prevalent CAD risk factor in this group of patients with DD was hypertension (53%), followed by hyperlipidemia (31%) and diabetes (22%). These data can help identify those patients who are asymptomatic in terms of DD who may be at risk for the condition. These patients should undergo an echocardiograph examination in order to rule out presence of DD, even if symptoms are not present.

Takotsubo cardiomyopathy: case report and review of the literature.

Takotsubo cardiomyopathy, also known as stress induced cardiomyopathy and transient left ventricular apical ballooning syndrome, is a rare syndrome that is characterized by a transient decrease in ejection fraction. This is accompanied by hypokinesis of the left ventricle and ballooning of the apex, with hypercontractile base and non-obstructive coronary artery disease. Takotsubo was first described in Japan in the early 1990's. It was named such due to the morphology of the apical ballooning that is similar in shape to a 'takotsubo', which is a pot with a round bottom and narrow neck used for trapping octopuses. Though most often described in Asians, reports of Takotsubo in Caucasian populations is becoming more common, possibly due to heightened awareness and detection. The most common presenting symptom of Takotsubo is acute chest pain mimicking myocardial infarction. Patients may also present with dyspnea, pulmonary edema and, more rarely, cardiogenic shock. Clinical symptoms are accompanied by transient left ventricular dysfunction. Despite clinical symptoms consistent with acute myocardial infarction, normal coronary arteries are usually detected upon cardiac catheterization. The case presented here is of an Asian woman who developed symptoms of acute myocardial infarction during a stressful hospital stay.

Platelet aggregation inhibition in patients receiving statins either fully or partially metabolized by CYP3A4.

Clopidogrel therapy is the standard for prevention of cardiovascular thrombotic events. Clopidogrel is converted to an active thiol by the cytochrome P450 CYP 3A4 and 2C19 enzymes. Recent studies suggest that statins metabolized by CYP3A4 attenuate the anti-aggregatory effect of clopidogrel. We evaluated the effect of CYP3A4-metabolized statins (atorvastatin, group 1) and partially-CYP3A4-metabolized statins (simvastatin, group 2) on platelet aggregation inhibition (PAI) when given concomitantly with clopidogrel as compared to patients who were statin naive (group 3). PAI was measured by PlateletWorks (Helena Laboratories ICHOR) using the platelet P2Y12 receptor agonist ADP (20 micromol). All patients were on clopidogrel therapy (75 mg/day). Non-responsiveness was defined as a PAI of < 35%. There was no statistical difference in mean PAI among groups; a higher prevalence of clopidogrel non-responders was noted in group 1 compared to group 3 (p=0.002). Multivariate analysis, adjusting for unequal presence of metabolic syndrome and hypertension, we found no statistical difference between groups. Our data suggests that statins, either fully or partially metabolized by CYP3A4, do not influence PAI when clopidogrel is used at 75 mg/day, even after adjusting for risk factors. We concluded that concomitant statins with clopidogrel therapy does not influence the effect of clopidogrel in PAI.

Prognostic significance of systolic blood pressure increases in men during exercise stress testing.

Our aim was to investigate whether exercise-induced increase in systolic blood pressure (BP) measured during exercise stress testing (EST) adds prognostic information to cardiovascular (CV) mortality. EST is ideally suited to evaluate the prognostic power of systolic BP; it not only measures systolic BP response to exercise but also provides information about exercise capacity and other EST variables, which may affect the peak systolic BP. The study population consisted of 6,145 consecutive patients who underwent symptom-limited EST. Using the median value of change in systolic BP from baseline, patients were grouped according to exercise-induced increases in systolic BPor=44 mm Hg (group B, n=3,083). Multivariate analysis was used to adjust for baseline differences between the 2 groups with CV mortality as the end point for follow-up. Six thousand one hundred forty-five men underwent EST with a mean follow-up of 6.6 years. During follow-up, 676 patients died of CV causes with an average annual CV mortality of 1.6%. CV mortality was significantly higher in group A than in group B (13.7% vs 8.2%, p<0.001). After adjusting for baseline differences in the 2 groups using multivariate analysis, an increase in systolic BP of or=44 mm Hg during EST was associated with a 23% improvement in survival over a mean follow-up of >6 years.

Systemic assessment of arterial wall structure and function in metabolic syndrome.

Metabolic syndrome (MetS) is thought to increase cardiovascular risk. The aim of this study was to investigate whether the MetS and its components are associated with parameters of arterial stiffness, flow mediated dilatation (FMD) of the brachial artery, carotid intima-media thickness (IMT) and the presence of carotid plaques (CP) in middle-aged subjects. One-hundred eighty-six asymptomatic volunteers (40-65 years-old, 86 males and 100 females) without clinically overt cardiovascular disease were examined. MetS was defined according to the International Diabetes Federation consensus. The prevalence of MetS was 32.8% (61 subjects). Augmentation index (Alx) and carotid-radial pulse wave velocity (PWV) as parameters of arterial stiffness were assessed by applanation tonometry. FMD (as endothelial function) was determined using high resolution B-mode ultrasonography, as were IMT and CP. PWV was significantly elevated in the MetS group (9.20 +/- 1.08 vs. 8.70 +/- 1.02, p = 0.003). FMD was significantly lower in the MetS group (5.32 vs. 6.45%, p = 0.018). There was no statistically significant difference in AIx between subjects with and without MetS (23.97 +/- 8.08 vs. 23.30 +/- 9.75, p = 0.248, respectively). Multiple regression analysis has shown that the presence of MetS was a significant (p = 0.005) determinant of PWV but not FMD. IMT* was higher in the MetS group (0.08 [0.07-0.1] vs. 0.07 [0.06-0.08] p < 0.001). The presence of arterial hypertension was related to AIx (R2 = 0.444, adjusted R2 = 0.434, p = 0.001) and PWV (R2 = 0.161, adjusted R2 = 0.152, coefficient p = 0.001). Furthermore, mean arterial pressure (MAP) itself was an independent predictor of AIx (R2 = 0.571, adjusted R2 = 0.562, p < 0.001) and PWV (R2 = 0.281, adjusted R2 = 0.269, p < 0.001). Glycemia had an impact on IMT (R2 = 0.027, adjusted R2 = 0.022, p = 0.026). The MetS was a significant predictor of the presence of carotid plaques (OR = 0.341, 95 % CI [0.173 - 0.673], p = 0.002). Blood pressure is the most important determinant of structure and function of arteries.

Methemoglobinemia and transesophageal echo.

Methemoglobin (MHb) is the oxidized form of Hemoglobin (Hb) containing iron in its ferric (Fe3+) rather than ferrous (Fe2+) state. Under physiologic conditions, diaphorase II accounts for only a small percentage of the red blood cell reducing capacity but can be pharmacologically activated by exogenous cofactors. Methemoglobinemia is an abnormal elevation of MHb levels resulting in impaired oxygen delivery to tissues as well as a left shift of the oxygen-Hb dissociation curve. We present the case of a 56-year-old female patient who underwent transesophageal echocardiography (TEE) prior to elective cardioversion. Prep for TEE included use of Hurricane spray. Twenty min after receipt, the patient's O2 saturation by pulse oximetry dropped from 100% to 86%; heart rate and blood pressure were unchanged. Physical exam revealed pallor, perioralcyanosis and acrocyanosis without tachypnea, respiratory distress, or jugular venous distension. A 100% non-rebreather mask provided no improvement. MHb was suspected and arterial blood gasses were drawn which was dark chocolate in appearance. Methylene Blue at 1 mg/kg over 5 minutes was administered empirically. ABG results were: pH 7.44/ CO2 40/ O2 315/ HCO2 26/ O2 sat 69%; MHb levels were 30.1% confirming the diagnosis of methemoglobinemia. This condition resolved within minutes. Though uncommon, MHb is the most Sported adverse event associated with topical benzocaine use. Untreated, it can lead to significant cardiopulmonary compromise, neurologic sequelae, and even death. Prompt recognition of this potentially life-threatening side-effect is essential in order to provide opportune treatment.

Nephropathy in critically Ill patients without preexisting renal disease.

Contrast-induced nephropathy (CIN) remains a common complication of radiographic procedures. Isovue (lopamidol) is a low-osmolality nonionic monomeric tri-iodinated water soluble agent widely used as a contrast medium in radiographic procedures for intravascular, intrathecal, and body cavity administration. The purpose of this study was to evaluate the effect of lopamidol on renal function in patients without any preexisting renal condition who were undergoing radiographic imaging with the iodine contrast. Seventy-five patients admitted to the Intensive Care Unit (ICU) had CT-scans with intravenous lopamidol contrast. All the patients had a normal serum creatinine before administration of the contrast media. Serum creatinine was recorded for three consecutive days after the CT-scan. The control group consisted of medical ICU patients that were not administered iodine contrast during their stay in the unit. There was no change from the baseline in the control group. A significant increase in serum creatinine was recorded in patients undergoing CT-scan with lopamidol contrast. In 18% of the patients, creatinine was elevated more than 25% from the baseline. This level of creatinine elevation indicated a significant decrease in glomerular filtration, and thus fulfilled the criteria for contrast-induced nephropathy. Our data demonstrates that iodine contrast media for CT in ICU patients without preexisting kidney disease can precipitate clearly measurable nephropathic changes.

Correlation between cardiac enzyme elevation and the duration of cardiopulmonary resuscitation.

Cardiovascular disease is the leading cause of death in the United States. Acute myocardial infarction (MI) is defined as necrosis of myocardial cells. Several studies have shown that cardiac markers are elevated after successful cardiopulmonary resuscitation (CPR) due to physical as well as electrical trauma. Correlation has never been established between an elevation in cardiac markers and patient age, the amount of trauma induced during resuscitation, or the duration of chest compression. Previous studies have determined that cardiac troponin (cTnl) is the most sensitive marker in cardiac injury. In this study, we hypothesized that the duration of CPR and the patient's age had a direct correlation with cardiac injury demonstrated as an elevation of cTnl. We analyzed retrospectively 81 patients that underwent successful CPR in an in-hospital setting. 13 patients were excluded from the analysis due to positive cTnl prior to cardiac arrest. Duration of CPR, as well as cTnl levels before and after cardiac arrest were recorded and analyzed in the remaining 68 patients. Patients with a negative cTnl after successful CPR (n=30) were stratified into Group A. The remaining patients (Group B) had a positive cTnl ranging from 2.2-31 ng/ml. The mean age and the mean duration of CPR in minutes were calculated and compared using t-Test analysis. There was no statistical difference in age between Group A and Group B. Patients in Group A had a mean CPR duration of 12.2 minutes, while patients in Group B had a mean CPR duration of 19.8 minutes (p < 0.02). We found that the duration of cardiopulmonary resuscitation was positively associated with the elevation of cardiac markers.

Etiology of cerebrovascular accidents in octogenarians.

Stroke is the third leading cause of death in the United States, after coronary heart disease and cancer. Many survivors are left with mental and physical impairment and require assistance with activities of daily living. Twenty-eight percent of patients with stroke are under 65 years of age. We analyzed retrospectively 213 elderly patients with the diagnosis of ischemic cerebrovascular event that were consecutively admitted to the stroke unit of our institution between January 2002 and December 2004. Patient age varied from 65 to 100 years (mean = 79.8 years), and there were 66.19% females and 33.81% males. We analyzed the head CT findings of all the patients and separated the patients into two groups based on the results. Patients in Group I had large infarcts on CT and extensive neurological deficits, while patients in Group II had small lacunar infarcts and minor neurological findings. The charts of all the patients were reviewed retrospectively and data on hypertension, diabetes mellitus, carotid stenosis, atrial fibrillation, left ventricular hypertrophy and anticoagulation were retrieved and analyzed. Our results showed that 35.6% (76) of the patients suffered a major stroke (Group 1) and the remainder 64.4% (137) suffered small lacunar strokes (Group 2). More than half (57.9%) of the patients in Group I were found to have atrial fibrillation and significant carotid stenosis (35.5%) and 22.4%), respectively. The remaining patients (28) were hypertensive and 12% had diabetes mellitus, but no extracerebral source of embolism was found. In Group II, only 13.1% were found to have atrial fibrillation or significant carotid stenosis, but all were hypertensive and 86% suffered from diabetes. Our results indicate that major strokes are less prevalent in the geriatric population than small lacunar strokes and tend to be more related to hypertension and diabetes.

Troponin I as a marker of doxorubicin induced cardiotoxicity.

Doxorubicin is a chemotherapeutic agent successfully used in the treatment of a wide range of cancers. However, with cumulative doses, doxorubicin also is known to have cardiotoxic effects, including cardiomyopathy and heart failure. Identification and quantification of myocardial cell damage has been a point of Controversy. We sought to identify these changes by measuring the levels of troponin I both 24 and 48 hr after the administration of doxorubicin as part of an antineoplastic treatment regimen. Thirty-eight patients scheduled to undergo treatment with doxorubicin were screened and approached for enrollment in the study. Thirty-one of them fulfilled all the inclusion criteria and also signed informed consent. All the patients enrolled in the study had blood drawn before the administration of doxorubicin and also 24 and 48 hr later. Electrocardiograms were performed prior to and 48 hr following the administration of chemotherapy. The dose of doxorubicin administered was calculated by the oncologist and ranged from 450 mg/m2-650 mg/m2 (mean 520 mg/m2). Only one patient was found to have en elevation of troponin levels both 24 and 48 hr (2.3 ng/mL and 2.1 ng/mL, respectively) after the administration of the drug. During that time, the patient denied any chest pain, shortness of breath or palpitations. Repeat ECG did not show any changes from the baseline. The remaining participants continued to maintain a troponin level of less than 0.3 ng/mL during the follow-up. In these patients, no electrocardiographic changes were noted in the follow-up ECG compared to the baseline; however, a slight drop in the ejection fraction without any impact on the clinical presentation was recorded. We concluded that the cTnl level does not change after the administration of doxorubicin, and thus cannot be used as a predictor of doxorubicin-induced cardiotoxicity.

Prolonged requirement for ventilatory support in a patient with Eskalith overdose.

Lithium (Eskalith) is commonly used in the treatment of depressive and bipolar affective disorders, in a population at relatively high risk for overdose. Lithium may help correct a chemical imbalance in the brain; however, it has a comparatively narrow therapeutic index. Thus, lithium intoxication is a frequent complication of chronic lithium therapy. The central nervous system (CNS) is the major organ system affected, although the renal, gastrointestinal (GI), endocrine, and cardiovascular (CV) systems also may be involved. Here we present a forty-two-year-old Caucasian female with altered mental status, inability to eat, speak or walk properly, with shaking and vomiting for three days. Past medical history was significant for hepatitis C and bipolar disorder. Vital signs were within normal limits. Physical exam revealed a patient with aphasia, tremor, and an expressionless face, able to make eye contact and move all four extremities. However, she was unable to follow commands and she expressed rigidity of extremities, mild tachycardia, and stupor. Severely elevated serum lithium levels were found. A diagnosis of severe lithium toxicity was made and the patient was admitted to the telemetry unit. Intravenous hydration with normal saline was initiated as the patient had normal kidney function, and urinary output was monitored. All psychotropic medications were held except for a benzodiazepine. In the meantime the patient developed acute respiratory distress, was intubated on clinical grounds and was transferred to the intensive care unit. Acute cardiogenic pulmonary edema and other causes of respiratory distress were ruled out; diagnosis of Adult Respiratory Distress Syndrome (ARDS) was made. After two months of mechanical ventilation, the patient was stabilized. Mental status, vital signs, and all laboratory parameters including thyroid function tests, normalized. The patient was transferred to a rehabilitation center. This is a rare case of ARDS associated with lithium intoxication.

Reactive oxygen species increased focal adhesion kinase production in pulmonary microvascular endothelial cells.

Focal adhesion kinase (FAK) is a 125 kDa protein tyrosine kinase (PTK) associated with focal adhesion in many cells, which plays a major role in the integrity of cytoskeletal structure. Reactive oxygen species produced during ischemia and reperfusion injury has been found to be an important mediator of signal transduction process. We found that low dose H2O2 induced increased FAK production in pulmonary microvascular endothelial cells, which could be blocked by cycloheximide (CHX), a protein synthesis inhibitor. Pulmonary endothelial cells were cultured on DMEM medium till 100% confluent. H2O2 was added at 100 uM for 30 min. The cells were collected and lysed, then immuno-blotted with anti-FAK antibody. After 30 min treatment, we found a 30%+/-6% (N=5) increase of FAK in H2O2 treated endothelial cells. This increase could be blocked by pretreatment of cells with CHX at 5 ug/ml for 60 min. In both groups, increased phosphorylation of ERK was observed. Immuno-fluorescence revealed increased staining of FAK in the peri-nuclear region of the H2O2 treated endothelial cells. These findings suggest that H2O2 activated MAP kinase pathway leading to increased FAK production at the protein level. FAK is a 125 kDa PTK associated with focal adhesion in many cells, and it plays a major role in the integrity of cytoskeletal structure. FAK is discretely localized to focal adhesions via its C-terminal focal adhesion-targeting (FAT) sequence. FAK is regulated by integrin-dependent cell adhesion and can control tyrosine phosphorylation of downstream substrates, like paxillin. The reactive oxygen species produced during ischemia and reperfusion injury has been found to be an important mediator of the signal transduction process. Although the signaling pathways leading to hydrogen peroxide induced endothelial monolayer permeability remain ambiguous, cytoskeletal proteins are known to be essential for maintaining endothelial integrity and regulating solute flux through the monolayer. Recent evidence has shown that H2O2 stimulates cytoskeleton reorganization, cell growth/proliferation, and DNA synthesis in various cells. In our previous study, we found a significantly increased amount of FAK in endothelial cells treated with low doses of H2O2. Mitogen-activated protein (MAP) kinases are a group of 30- to 110-kDa serine/threonine kinases. MAPKs belong to the group of kinases that are rapidly activated in response to growth factor stimulation. This family of MAPKs includes ERK, and ERK2. The activated MAPK can translocate to the nucleus where it can regulate transcription factors. Activation of p44 and p42 extracellular signal-regulated protein kinases (ERK1 and ERK2) is an important step in the cascade leading to cell growth and proliferation. In order to determine the mechanism of increased FAK production, we investigated the relationship of FAK production and ERK activation.

Ischemia induced focal adhesion kinase cleavage in rat lung.

Focal adhesion kinase (FAK), a 125 kDa protein, is located at the focal adhesion sites that stabilize endothelial cells on the matrix. Ischemic stimuli cause FAK cleavage and FAK depletion from focal adhesion sites. To test this hypothesis under ischemic conditions, we established an isolated rat lung that we ventilated at 40 inflations/min at inspiratory and expiratory pressures of 10 and 3 cm H2O, respectively. After 5 min of blood perfusion at pulmonary arterial and left atrial pressures of 13 and 3 cm H2O respectively, we either stopped (ischemic group, n=10) or continued (perfused group, n=10) perfusion for 2 hr. We then recovered endothelial cells from each lung, using our previously reported magnetic cell separation method. The endothelial lysates were separated into cytosol and membrane fractions, then immunoprecipitated and blotted with anti-FAK, and anti-phospho-FAK antibody. In ischemic as compared to perfused lungs, immunoblotting with anti-FAK antibody revealed a greater prominence of bands at 125 kDa as well as at cleavage products 80, 70 and 44 kDa in the cytosol fraction. Immuno-blotting with anti-phosphotyrosine antibody revealed decreased enhancement of bands at 80, 70 and 44 kDa, also at 125 kDa in the cytosol fraction. We propose that during lung ischemia, FAK is dephosphorylated, cleaved and translocated to the cytosol. This first evidence of the involvement of FAK in lung ischemia suggests that destabilization of focal adhesions may underlie endothelial barrier deterioration, contributing to increased vascular permeability in ischemic lung injury.

Cardiac rate normalization in chronic atrial fibrillation: comparison of long-term efficacy of treatment with amiodarone versus AV node ablation and permanent His-bundle pacing.

Chronic atrial fibrillation (AF) is a common arrhythmia with significant morbidity and mortality. AF has been the subject of considerable attention and intensive clinical research in recent years. Current opinion on the management of AF favors the restoration and maintenance of normal ventricular rhythm. This has several potential benefits, including the alleviation of arrhythmia-associated symptoms and hemodynamic improvements. Maintenance of frequents normalization of ventricular rhythm (NVR) can be achieved with antiarrhythmic drug therapy or with AV node radiofrequency ablation (RFA) and permanent ventricular pacing. Recent interest has focused on the use of class III antiarrhythmic agents, such as amiodarone hydrochloride. This investigation compared amiodarone to AV node RFA and permanent pacing of the His-bundle area in maintaining NVR in patients with resistant chronic AF. After 12 months of treatment with amiodarone (200 to 400 mg/d) 30 % of patients remained in NVR, 30 % were in transitional phase of improvement, and 40 % showed negative effect. Only a few patients in this group developed ocular or hepatic side effects. On one year follow-up was achieved in 100 % of cases without any clinically significant side effects being seen. In conclusion, analysis of the results of this study suggests that low-dose amiodarone is well tolerated in the management of chronic AF in a selected patient population. The more aggressive interventional radiofrequency ablation technique is significantly more effective and more reliable in the long-term clinical treatment of drug-resistant AF.

Comparison of clinical outcomes using stents versus no stents after percutaneous coronary intervention for proximal left anterior descending versus proximal right and left circumflex coronary arteries.

Previous studies have demonstrated that proximal left anterior descending (LAD) stenoses have higher rates of restenosis after angioplasty than stenoses in other coronary segments. Stenting strategies may reduce this high rate of LAD restenosis. The study population included 1,289 patients with proximal coronary artery stenoses treated with percutaneous coronary interventions (PCI) with or without stents for single-vessel coronary disease between 1994 and 1999. Patients were divided into 4 groups: non-stent PCI in the proximal LAD artery (n = 168), non-stent PCI in proximal right/circumflex artery (n = 217), stent in the proximal LAD artery (n = 364), and stent to proximal right/circumflex artery (n = 540). Procedural success was higher in the stenting groups, but there were no significant differences in the major in-hospital events between the different lesion locations among the groups. At 1-year follow-up, there was no difference in mortality or myocardial infarction between the groups. There was no significant difference in the rate of target lesion revascularization (TLR) in the patients with proximal LAD stents compared with the patients with proximal right/circumflex coronary artery stents (10.1% vs 13.8%, p = 0.11). In the patients who did not receive stents with proximal narrowings, there was a significant increase in TLR in the LAD group compared with the right/circumflex group (21.1% vs 12.5%, p = 0.04). Thus, patients with proximal stenoses treated with non-stenting strategies have lower procedural success than those treated with stenting strategies; the patients with proximal LAD non-stent PCI have significantly higher rates of clinical restenosis than patients with proximal right and circumflex stenoses. A stenting strategy for proximal LAD stenoses appears to attenuate the differences of clinical restenosis noted after non-stent PCI.