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A major hypothesis regarding the cause of chronic fatigue syndrome (CFS) is immune dysregulation, thought to be reflected in upregulated proinflammatory cytokines leading to the symptoms that are characteristic of this illness. Because the symptoms worsen with physical exertion or sleep loss, we hypothesized that we could use these stressors to magnify the underlying potential pathogenic abnormalities in the cytokine systems of people with CFS. We conducted repeat blood sampling for cytokine levels from healthy subjects and CFS patients during both postexercise and total sleep deprivation nights and assayed for protein levels in the blood samples, mRNA activity in peripheral blood lymphocytes (PBLs), and function in resting and stimulated PBLs. We found that these environmental manipulations did not produce clinically significant upregulation of proinflammatory cytokines. These data do not support an important role of immune dysregulation in the genesis of stress-induced worsening of CFS.

Background Carvedilol has improved the symptomatic status of patients with moderate to severe heart failure in single-center studies, but its clinical effects have not been evaluated in large, multicenter trials. Methods and Results We enrolled 278 patients with moderate to severe heart failure (6-minute walk distance, 150 to 450 m) and a left ventricular ejection fraction ≤0.35 at 31 centers. After an open-label, run-in period, each patient was randomly assigned (double-blind) to either placebo (n=145) or carvedilol (n=133; target dose, 25 to 50 mg BID) for 6 months, while background therapy with digoxin, diuretics, and an ACE inhibitor remained constant. Compared with placebo, patients in the carvedilol group had a greater frequency of symptomatic improvement and lower risk of clinical deterioration, as evaluated by changes in the NYHA functional class ( P =.014) or by a global assessment of progress judged either by the patient ( P =.002) or by the physician ( P P P =.029). In contrast, carvedilol therapy had little effect on indirect measures of patient benefit, including changes in exercise tolerance or quality-of-life scores. The effects of the drug were similar in patients with ischemic heart disease or idiopathic dilated cardiomyopathy as the cause of heart failure. Conclusions These findings indicate that, in addition to its favorable effects on survival, carvedilol produces important clinical benefits in patients with moderate to severe heart failure treated with digoxin, diuretics, and an ACE inhibitor. (Circulation. 1996;94:2793-2799.)

Cigarette smoking is a major risk factor for the development of coronary artery disease and its complications. Nicotine is one of the major substances that contributes to the pharmacologic activity of cigarette smoke, its toxicity, as well as its addictive nature. Strategies have been developed that utilize nicotine as a replacement substance in motivated patients who wish to stop smoking. Studies have shown that nicotine replacement therapy can be used safely in patients with known coronary artery disease.

Vesnarinone is a new and novel inotropic drug that has unique and complex mechanisms of action. It inhibits phosphodiesterase, thereby leading to increased intracellular calcium, and also affects numerous myocardial ion channels, resulting in the prolongation of the opening time of sodium channels and the decrease in the delayed outward and inward rectifying potassium current. In vitro, it has also demonstrated significant effects on cytokine production, which may account for some of its observed clinical benefits. Hemodynamic studies in humans with congestive heart failure reveal that vesnarinone can improve ventricular function. Placebo-controlled studies in large numbers of patients with heart failure have suggested a morbidity and mortality benefit with a 60 mg daily dose. There is increased mortality with vesnarinone at the 120 mg daily dose, however, suggesting a narrow therapeutic window for the drug. Its predominant toxic side effect is a 2% incidence of reversible neutropenia.

Cardiac tamponade is a relatively uncommon complication following Permanent Pacemaker (PPM) implantation. Therefore, limited data exists regarding the predictors of tamponade among recipients of this procedure. We sought to identify predictors of cardiac tamponade from PPM implantation and

Uremic cardiomyopathy is responsible for high morbidity and mortality rates among patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD); however, the early implementation of hemodialysis may halt its progression. Nonconventional hemodialysis, such as frequent hemodialysis, appears to have an advantage over conventional hemodialysis. Kidney transplantation has been shown to reverse uremic cardiomyopathy and to confer a significant survival advantage over hemodialysis. Targeting future therapies at the underlying cellular mechanisms of uremic cardiomyopathy may finally start to reduce the burden of uremic cardiomyopathy in the CKD and ESRD population.

During a cardiac evaluation prior to liver transplantation, a 51-year-old man with hepatitis C and cirrhosis was found to have nonischemic cardiomyopathy-a condition that would have made him ineligible for liver transplantation. Right ventricular biopsy revealed extensive cardiac hemosiderosis. Despite the elevated levels of serum ferritin, the patient had no history of multiple red blood cell transfusions; moreover, genetic testing for hereditary hemochromatosis was negative for the HFE mutations C282Y and H63D. Chelation therapy was considered for this patient, to reduce the cardiac iron deposits. However, before a course of treatment was established, the patient's clinical condition worsened, and chelation therapy was no longer feasible. He was referred for combined heart and liver transplantation. Cardiac iron deposition can be diagnosed readily using right ventricular biopsy or T2* magnetic resonance imaging. Early detection may allow time for intensive chelation therapy, which might, in turn, reverse the myopathic process. Improved cardiac function should improve cirrhosis patients' chances to be placed on the liver transplant waiting list and ultimately optimize transplantation outcomes.

The purpose of this study was to compare the efficacy and safety of intracoronary (IC) nitroprusside and intravenous adenosine (IVA) for assessing fractional flow reserve (FFR).IV infusion of adenosine is a standard method to achieve a coronary hyperemia for FFR measurement. However, adenosine is expensive, causes multiple side effects, and is contraindicated in patients with reactive airway disease. Sodium nitroprusside (NTP) is a strong coronary vasodilator but its efficacy and safety for assessing FFR is not well established.We compared FFR response and side effects profile of IC NTP and IVA. Bolus of NTP at a dose of 100 μg and IVA (140 μg/kg/min) were used to achieve coronary hyperemia.We evaluated 75 lesions in 53 patients (60% male) mean age 61.6 ± 13.9 years. Mean FFR after NTP was similar to FFR after adenosine (0.836 ± 0.107 vs. 0.856 ± 0.106; P = 0.26; r = 0.91, P0.001). NTP induced maximal stable hyperemia within 10 sec (mean: 6.4 ± 1) which lasted consistently between 38 and 60 sec (mean 51 ± 7.5). NTP caused significant (14%), but asymptomatic decrease in mean blood pressure which returned to baseline within 60 sec. Adenosine caused shortness of breath in 26%, headache and flushing in 19%, and transient second degree heart block in 6% of patients. No adverse symptoms were reported after NTP.IC NTP is as effective as IVA for measuring FFR. NTP is better tolerated by patients. Since NTP is inexpensive, readily available, well tolerated, and safe, it may be a better choice for FFR assessment.

The inability to achieve 85% of the maximum predicted heart rate (MPHR) on dobutamine stress echocardiography (DSE) is defined as chronotropic incompetence and is a predictor of major cardiac events after orthotopic liver transplantation (OLT). The majority of patients with end-stage liver disease (ESLD) receive beta-blockers for the prevention of variceal bleeding. In these patients, it is impossible to determine whether chronotropic incompetence is secondary to cirrhosis-related autonomic dysfunction or is merely a beta-blocker effect. We evaluated the usefulness of the maximum achieved heart rate (MAHR) and the heart rate reserve (HRR) in the detection of chronotropic incompetence in ESLD patients on beta-blocker therapy before DSE. We also evaluated the usefulness of a new index, the modified heart rate reserve (MHRR), in diagnosing chronotropic incompetence and predicting major cardiovascular adverse events after OLT. The study population consisted of 284 ESLD patients. The mean values of MAHR (expressed as a percentage of 85% of MPHR) and HRR were significantly lower for patients on beta-blockers versus patients off beta-blockers [97.1% versus 101.6% (t = 5.01, P < 0.001) and 71.7% versus 77.3% (t = 4.03, P < 0.001), respectively], whereas the values of MHRR were similar in patients on beta-blockers and patients off beta-blockers [102.3% versus 102.1% (t = 0.04, P = 0.97)]. A regression analysis showed a significant association of MAHR (P < 0.001) and HRR (P < 0.001) with beta-blockers, whereas MHRR was not associated with beta-blocker treatment (P = 0.92). MAHR and HRR were found to have no value for diagnosing chronotropic incompetence in ESLD patients. MHRR was not affected by beta-blocker therapy. Patients who developed heart failure (HF) and myocardial infarction (MI) after OLT had significantly lower MHRR values according to pretransplant DSE. MHRR was significantly associated with the subsequent development of HF (P = 0.01) and MI (P = 0.01) after OLT. MHRR may be useful for the determination of the target heart rate for stress testing, the diagnosis of chronotropic incompetence, and the prediction of adverse cardiac events after OLT. Liver Transpl 18:355–360, 2012. © 2012 AASLD.

High-risk cardiac patients, especially those with severe coronary artery disease, are prone to ischemic, arrhythmic and heart failure complications during urgent or emergent noncardiac surgery. The American and European guidelines endorse selective revascularization by either coronary artery bypass grafting or percutaneous coronary intervention in symptomatic ischemic patients prior to major elective surgery. However, conventional revascularization may not be suitable for certain patients requiring emergent or urgent surgery. Reported are two representative cases in which severely ischemic patients were bridged uneventfully through moderate-risk surgery by using prophylactic intra-aortic balloon pump (IABP). Prophylactic IABP should be considered for the support of ischemic patients who are severely symptomatic or hemodynamically unstable undergoing moderate-high risk surgery, who are not suitable for preoperative revascularization. This therapeutic option should be acknowledged in the relevant guidelines.

[Figure][1] [![Graphic][3] ][3][![Graphic][4] ][4] A 49-year-old woman with exertional chest pain and a systolic murmur at the right upper sternal border radiating to both carotids had a hypercontractile left ventricle (LV) and a 77 mm Hg peak pressure gradient between the LV

Heart failure (HF) is a syndrome characterized by high mortality, frequent hospitalization, reduced quality of life, and a complex therapeutic regimen. Knowledge about HF is accumulating so rapidly that individual clinicians may be unable to readily and adequately synthesize new information into effective strategies of care for patients with this syndrome. Trial data, though valuable, often do not give direction for individual patient management. These characteristics make HF an ideal candidate for practice guidelines. The 2010 Heart Failure Society of America comprehensive practice guideline addresses the full range of evaluation, care, and management of patients with HF.

We describe a patient with an infrequent combination of variants in both the right and the left coronary arterial ostia, namely a combination of two separate right coronary artery (RCA) ostia from the aorta, and an anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA). To our knowledge, such a combination has not been previously reported. Based on published statistics for individual variants, such a combination is expected to occur approximately once for every 500,000 to one million live births. ALCAPA and dual RCA anatomy was characterized in our patient by echocardiography, conventional angiography, and multidetector computed tomography before and after Takeuchi repair.

The goal of this study was to evaluate the impact of the STAT-MI (ST-Segment Analysis Using Wireless Technology in Acute Myocardial Infarction) network on outcomes in the treatment of patients presenting with ST-segment elevation myocardial infarction (STEMI).Shortening door-to-balloon (D2B) time remains a national priority for the treatment of STEMI. We previously reported a fully automated wireless network (STAT-MI) for transmission of electrocardiograms (ECGs) for suspected STEMI from the field to offsite cardiologists, allowing early triage with shortening of subsequent D2B times. We now report the impact of the STAT-MI wireless network on infarct size, length of hospital stay (LOS), and mortality.A fully automated wireless network (STAT-MI) was developed to enable automatic 12-lead ECG transmission and direct communication between emergency medical services personnel and offsite cardiologists that facilitated direct triage of patients to the cardiac catheterization laboratory. Demographic, laboratory, and time interval data of STAT-MI network patients were prospectively collected over a 33-month period and compared with concurrent control patients who presented with STEMI through non-STAT-MI pathways.From June 2006 through February 2009, 92 patients presented via the STAT-MI network, and 50 patients presented through non-STAT-MI pathways (control group). Baseline clinical and demographic variables were similar in both groups. Overall, compared with control subjects, STAT-MI patients had significantly shorter D2B times (63 [42 to 87] min vs. 119 [96 to 178] min, U = 779.5, p0.00004), significantly lower peak troponin I (39.5 [11 to 120.5] ng/ml vs. 87.6 [38.4 to 227] ng/ml, U = 889.5, p = 0.005) and creatine phosphokinase-MB (126.1 [37.2 to 280.5] ng/ml vs. 290.3 [102.4 to 484] ng/ml, U = 883, p = 0.001), higher left ventricular ejection fractions (50% [35 to 55] vs. 35% [25 to 52], U = 1,075, p = 0.004), and shorter LOS (3 [2 to 4] days vs. 5.5 [3.5 to 10.5] days, U = 378, p0.001).A fully automated, field-based, wireless network that transmits ECGs automatically to offsite cardiologists for the early evaluation and triage of patients with STEMI shortens D2B times, reduces infarct size, limits ejection fraction reduction, and shortens LOS.

Ectopic origin of the right coronary artery (RCA) occurs in approximately 1.0% of studied populations. We investigated the prevalence and location of ectopic RCAs among patients undergoing coronary angiography (CA) and assessed its effects on resource utilization.Cases of ectopic RCAs were prospectively collected over 21 months among patients undergoing cardiac catheterization at a University Hospital. "Ectopic RCA" was defined as a RCA originating outside the posterior two-thirds of the right coronary sinus.The study population included 2,120 patients, of which 23 (1.1%) had ectopic RCAs. Of these, 15 (65%) originated from the anterior third of the right sinus, while 8 (35%) originated from the anterior half of the left sinus. Mean procedure and fluoroscopy times were 60 +/- 33 and 15 +/- 12 minutes (min) for the former, and 78 +/- 35 and 31 +/- 20 min for the latter, while mean contrast volume for CA was 112 +/- 62 ml and 192 +/- 85 ml, respectively. 26% required a second CA or a second intervention to image the RCA.Ectopic RCAs pose a clinical problem, consuming time and resources. The search for an ectopic RCA should have90 degree boundaries limited to the anterior third of the right sinus and anterior half of the left sinus.

It is commonly postulated that neurologic complications of atrial myxomas are due to either direct tumor embolization or mycotic aneurysm of cerebral vasculature or rupture of mycotic aneurysms of cerebral arteries. However, the authors report the case of 63-year-old woman with a large left atrial myxoma whose progressive left-sided weakness was due to a different neurologic mechanism, namely, multiple bleeding cavernous malformations, which were visualized by magnetic resonance imaging of the brain. Cerebral cavernous malformations coexist with mesenchymal anomalies of other organs, including the liver, kidneys, and retinas. To the best of the authors' knowledge, this is only the second reported case of coexistent cerebral cavernous malformations and atrial myxoma.

BACKGROUND The vasodilatory response to local specific type III phosphodiesterase inhibition with amrinone was evaluated before and immediately after local administration of digoxin in 14 patients with severe congestive heart failure (CHF). METHODS AND RESULTS A 3F polyethylene catheter was inserted into the common femoral artery for drug administration and pressure monitoring. Mean blood flow velocity (MBFV) was continuously determined in the superficial femoral artery by transcutaneous Doppler ultrasonography. After intra-arterial administration of 10 mg amrinone, group MBFV increased from 7.7 +/- 1.4 to 16.0 +/- 2.1 cm/sec (p less than 0.05, n = 10). Local administration of 20 micrograms digoxin, which was infused over 20 minutes, did not alter group MBFV (i.e., 8.2 +/- 1.6 versus 7.6 +/- 1.5 cm/sec; p = NS, n = 10). The second administration of 10 mg amrinone, which immediately followed completion of local digoxin infusion, increased group MBFV but to a lesser extent than that produced by the first amrinone administration (i.e., 11.9 +/- 1.9 versus 16.0 +/- 2.1 cm/sec; p less than 0.05, n = 10). When placebo was administered instead of digoxin, group MBFV was similar after the first and second administrations of amrinone (i.e., 15.3 +/- 3.3 versus 15.6 +/- 3.8 cm/sec; p = NS, n = 4). CONCLUSIONS Although local administration of digoxin did not significantly alter baseline vascular tone in patients with CHF, it substantially decreased the direct vasodilatory effect induced by specific type III phosphodiesterase with amrinone.

We report the case of an enormous right atrial hemangioma in an asymptomatic 42-year-old woman. The diagnosis was made by echocardiogram after the patient was found to have an abnormal EKG during a routine medical exam. The hemangioma is the largest described in English literature. The tumor was surgically resected and the patient did well postoperatively. In this case report, we discuss the discovery of the tumor and treatment of our patient. A brief discussion of cardiac hemangiomas follows.

Cardiogenic shock (CS) accompanying myocardial infarction carries a case fatality rate of 40–50%. Profound myocardial dysfunction is partially reversible, and possibly related to a state of inflammatory storm accompanied by nitric oxide (NO) overproduction. CS survivors enjoy satisfactory longevity and quality of life. The focus of this review is to describe the available data regarding NO synthase (NOS) inhibitors in CS. In view of supportive evidence from mammalian research (inducible-NOS-knockout mice are less susceptible to ischemic and reperfusion injury), therapies mitigating NO overproduction were tested in human CS subjects. Human randomized clinical trials project excellent safety but lack of efficacy. Although the Phase III, multicenter, prospective, randomized, double-blind, placebo-controlled Study to Assess the Safety and Efficacy of Tilarginine Acetate (L-NG-monomethyl arginine citrate [L-NMMA]) in CS (TRIUMPH) trial demonstrated lack of clinical benefit of 5-h infusion of L-NMMA in CS, major design issues regarding the optimal timing, dosing, duration and NOS inhibitor need to be addressed prior to rendering this therapy ineffective.

Coronary perforation is a rare, unpredictable and dreaded complication of percutaneous coronary Intervention. With Ellis Grade 3 perforations the only effective treatment includes temporary balloon occlusion of the perforated coronary artery and placement of JOSTENT GraftMaster stent to cover the perforation. The authors describe coronary perforation during proximal right coronary artery (RCA) stenting, resulting in immediate cardiogenic shock. The patient was treated with temporary balloon occlusion of the RCA, reversal of anti-coagulation, sealing of the perforation with a GraftMaster stent, inotropes, intra-aortic balloon counterpulsation (IABC) and surgical drainage the pericardial space. The authors describe the rational of their therapeutic strategy. The methodology and pitfalls of GraftMaster deployment, in patients with massive coronary perforation are discussed. This report also emphasizes, that as opposed to manufactures instructions and all previous manuscripts, GraftMaster can be easily deployed via conventional 6F guiding catheters with internal diameter 0.070 inch (1.8 mm).

Automated contrast injectors (ACIs) are widely employed in interventional cardiology, radiology and neurology. Information regarding the specifications of advanced ACIs and the appropriate injection settings of these devices is limited in the medical literature. This review describes the specifications of the most widely used ACIs and provides appropriate recommendations for injection settings for the various angiographic studies. These recommendations are based on expert consensus and commercial experience regarding characteristics of devices, catheters and contrast. The suggested settings were not subject to rigorous comparative clinical assessment. This review should increase the familiarity, comfort and appreciation of safety among ACI users.

We report a case of a 52-year-old man with multiple myeloma and rapidly progressive heart failure who died unexpectedly from a probable arrhythmia. Postmortem examination revealed infiltrative amyloid cardiomyopathy, a rare cause of predominantly diastolic myocardial disease. Cardiac amyloidosis should be considered in any patient presenting with congestive heart failure, preserved systolic function, and a discrepancy between a low QRS voltage on electrocardiography and an apparent left ventricular hypertrophy on sonogram. The pattern of left ventricular diastolic dysfunction changes during the course of amyloidosis and the classically described restrictive physiology occurs only in advanced stages of the disease.

Until October 2008, coronary drug-eluting stents with a diameter of ≤2.5 mm were not approved by the FDA. Target vessels of ≤2 mm in diameter pose a major challenge in view of high restenosis rates when stented bare metal stents (BMS) are used and distal edge dissection when oversized stents are deployed. Described is a method (“funneling”) to optimize stenting of small vessels. This strategy combines stenting the distal part of the lesion with short (8–12 mm length) 2-mm bare metal stent while stenting with a larger-diameter (≥2.5 mm) drug-eluting stent (DES) with considerable DES–BMS overlap (leaving only the distal 4–6 mm of the BMS not overlapped by a DES). The two stents create a funnel that is for the most part drug eluting. With funneling, both drug elution and larger diameter are attained, minimizing both edge dissection and restenosis.

A 59-year-old woman with hypertension presented with right flank pain. Magnetic resonance imaging of the abdomen revealed a 9 cm × 8 cm right renal mass and a filling defect (tumour extension) in the inferior vena cava (IVC), with protrusion into the right atrium (Figure 1). Figure 1) Magnetic resonance imaging of the abdomen showing a 9 cm × 8 cm right renal mass and a filling defect (tumour extension) in the inferior vena cava (thin arrow) with protrusion into the right atrium (thick arrow) Transthoracic echocardiography showed a large mobile mass (Figure 2) protruding from the IVC into the right atrium. The patient underwent radical right nephrectomy and excision of the mass from the IVC and right atrium. Microscopic examination of the renal mass and its intracaval and intracardiac extension demonstrated renal cell carcinoma of clear cell type. The patient remained stable on follow-up examination. Figure 2) Transthoracic echocardiogram showing a large mobile mass (arrow) protruding from the inferior vena cava (IVC) into the right atrium. Ao Ascending aorta; RV Right ventricle Malignant renal tumours represent approximately 2% of all malignant neoplasms (1). Patients with renal cell carcinoma and extension into the atrium have a significantly worse prognosis than those with other levels of vena caval involvement (2). Echocardiography plays an important role in diagnosing tumour clot extension into the right heart through the IVC.

Background: We previously reported our early (initial 6 month) experience using a fully automated wireless network to shorten door to intervention (D2I) times. Later experience allowed for further refinement of this network. Early D2I times are expected to result in smaller infarcts and decreased lengths of stay. Methods: A fully automated wireless network that facilitates simultaneous 12-lead ECG transmission from emergency medical services (EMS) personnel in the field to the Emergency Department (ED) and offsite cardiologists via smart phones. This allows direct communication between offsite cardiologist and EMS and facilitates patient triage directly to the cath lab. Demographic, laboratory and time interval data were prospectively collected over a 23-month period and compared to calendar year 2005 data. Early experience (first 6 months) was compared to later experience. Results: From June 2006 through April 2008, 242 ECGs with suspected ST segment elevation myocardial infarction (STEMI) were transmitted via the STAT-MI network. Compared with 2005 data, door to cardiology notification time was reduced from 61.4 minutes (min) to −15.8 min (p < 0.001), door to arterial access time decreased from 108.1 to 42.1 min (p < 0.0001), door to intervention (D2I) time decreased from 145.7 to 68.8 min (p = 0.00001), hospital length of stay decreased from 5.4 ± 4.5 days to 4.1 ± 5.0 days (p < 0.29), and troponin elevation decreased from 106.4 ng/ml to 73.9 ng/ml (p < 0.19). The magnitude of timesavings was similar regardless of time of presentation, though D2I times were longer during “off” hours (after 5pm and weekends) as compared to “on” hours (85.7 min vs. 51.8 min P=0.001). Protocol refinements introduced over the first 6 months further shortened D2I times; 87 min vs 65 min in the first 6 months and in the subsequent 17 months respectively (p = 0.09). Conclusions: A fully automated wireless network that transmits ECGs simultaneously to the ED and offsite cardiologists for the early evaluation and triage of patients with STEMI markedly and consistently shortened D2I times. A strong positive trend in outcome measures was also observed with reduced length of stay and smaller infarct size. There was a 6 month learning curve to fully realize the benefits of this new automated system.

MGuard is a bare-metal stent covered by an ultrathin polymer mesh sleeve on its external surface, designed to reduce embolization during coronary, cerebrovascular and peripheral interventions.To evaluate the feasibility and safety of MGuard-based percutaneous coronary interventions (PCIs) of human native coronary arteries (NCs) and coronary vein grafts (VGs).MGuard-based PCI executed by 2 centers with postprocedural clinical and laboratory monitoring; including creatinine phosphokinase (CPK), troponin, electrocardiography and 6-month angiographic follow up. The primary endpoint was 30-day major adverse cardiac events (MACE) including cardiac death, myocardial infarction, stent thrombosis and repeat target lesion revascularization. The secondary endpoint was device and procedural success.Twenty-nine patients with a mean age of 68.1 +/- 12 years were enrolled. The mean VG age (n = 17) was 12.6 years (range 8-19). All patients received heparin, clopidogrel and aspirin, while none received bivalirudin, glycoprotein IIb/IIIa inhibitors (GPIs) or an embolic protection device (EPD). Device and procedural success were 100% and 96.5%, respectively. One patient experienced a procedure-related CPK rise. No MACE were reported at 1 month.MGuard-based PCI of NCs and VGs appears encouraging, especially in view of unfavorable patient and lesion characteristics. Both efficacy and safety need to be further established in larger-scale studies with longer follow-up periods.

M-Guard is an ultra-thin polymer mesh sleeve attached to the external stent surface. It is designed to minimize distal embolization during coronary, renal, carotid and vein graft stenting. The polymer net could also serve as a platform for more uniform drug delivery.To evaluate coronary M-Guard stent deliverability and safety (stent thrombosis and restenosis) in comparison to bare-metal stents (BMS) in a porcine model of percutaneous coronary interventions (PCIs).Under general anesthesia using percutaneous technique, 6 swine received a total of 18 coronary stents: 5 BMS and 13 M-Guard-BMS. Quantitative coronary angiography (QCA) was obtained immediately prior to and post-PCI, and at 30 days post-stenting. At 30 days, all animals were sacrificed and hearts were sent to a core lab for coronary histology and histomorphometry. Primary endpoints were 30-day QCA percent diameter stenosis, late luminal loss and minimal luminal diameter (MLD). Secondary endpoints were procedural success, 30-day mortality and stent thrombosis. Exploratory endpoints were histology and histomorphometric analysis performed at 30 days on M-Guard stented segments.All stents were delivered successfully. There were no procedural complications or porcine morbidity or mortality at 30 days. The M-Guard and BMS displayed similar results of MLD, late luminal loss and percent diameter stenosis at 1 month.When compared to BMS, PCI with M-Guard-BMS is feasible, safe and yields similar inflammatory and restenotic response.

Asymptomatic subclavian vein occlusion following insertion of a permanent pacemaker (PPM) or implantable cardioverter-defibrillator (ICD) is not uncommon. We report a case of a dual-chamber PPM in a patient with an unrecognized left subclavian vein occlusion who developed massive left arm edema following ipsilateral implantation of an arteriovenous (AV) hemodialysis graft. We recommend that patients with pre-existing PPM or ICD leads who are in need of vascular access for hemodialysis should have the AV shunts placed in the contralateral arm. If this is unavoidable, then preoperative subclavian vein screening for patency should be mandatory, even in asymptomatic patients. Sonography is an appropriate initial test in such a situation. © 2007 Wiley Periodicals, Inc. J Clin Ultrasound, 2008

Reported are two cases in which stent protrusion from the right coronary ostium into the aorta caused considerable difficulty in interventions. Two different methods were applied to overcome this problem. In the first (elective) case a new orifice was created at the side of the protruding stent. In the second case (acute inferoposterior and right myocardial infarction associated with complete heart block, recurrent ventricular fibrillation and shock), a new track was created underneath the underexpanded protruding stent, and the protruding stent was crushed under a new stent. Stents protruding from the right coronary artery into the aorta may present a considerable challenge during interventions, which can be managed by certain technical modifications.

beta-blockade has a therapeutic role across the continuum of patients with heart failure (HF), with a demonstrated mortality benefit in stage II and III HF. Concerns regarding initiation and uptitration linger as patients with resting bradycardia, pulmonary, or vascular disease are often unnecessarily excluded from receiving therapy. We will review the risk data on beta-blockade and offer therapeutic strategies to help overcome residual barriers to the initiation and uptitration of this important therapy in patients with HF.

We present a case of AIDS-related Burkitt's type cardiac lymphoma in a middle-aged woman with Epstein-Barr virus infection and profound immunodeficiency. The original features of our case include left ventricular location, female sex, and the use of contrast echocardiography to help establish the diagnosis. © 2007 Wiley Periodicals, Inc. J Clin Ultrasound, 2007

Left ventricular (LV) free wall rupture is a serious and deadly phenomenon, usually seen as a complication of myocardial infarction (MI). Rapid recognition of LV free wall rupture and treatment is crucial to survival. Although performing pericardiocentesis in such patients is risky, it can be

ST segment Elevation Myocardial Infarction (STEMI) affects 160,000 annually in the US. Guidelines direct immediate revascularization and adjunctive medical therapies. Yet STEMI victims remain at risk for infarct expansion, heart failure, reinfarction, repeat revascularization and death. In pre

We report a case of a 56-year-old man with traumatic aortic rupture (TAR) sustained in a motor vehicle accident diagnosed by helical computed tomography, aortography, and transesophageal echocardiography. A large majority of patients with TAR never make it to the hospital, and for those who do, a timely diagnosis is critical for survival. We discuss the merits and pitfalls of the three imaging modalities.

We present the case of a patient with severe symptomatic pulmonary hypertension due to rheumatic mitral valve disease who was refractory to traditional therapies, including prostacyclin. Therapy with continuous nesiritide infusion resulted in significant and sustained decreases in pulmonary vascular resistance, an improvement in renal function, and the maintenance of euvolemia.

Nearly 1 million hospitalizations for chronic heart failure occur yearly in the United States, with most related to worsening systemic congestion. Diuretic use, the mainstay therapy for congestion, is associated with electrolyte abnormalities and worsening renal function. In contrast to diuretics, the vasopressin antagonist tolvaptan may increase net volume loss in heart failure without adversely affecting electrolytes and renal function.To evaluate the short- and intermediate-term effects of tolvaptan in patients hospitalized with heart failure.Randomized, double-blind, placebo-controlled, parallel-group, dose-ranging, phase 2 trial conducted at 45 centers in the United States and Argentina and enrolling 319 patients with left ventricular ejection fraction of less than 40% and hospitalized for heart failure with persistent signs and symptoms of systemic congestion despite standard therapy.After admission, patients were randomized to receive 30, 60, or 90 mg/d of oral tolvaptan or placebo in addition to standard therapy, including diuretics. The study drug was continued for up to 60 days.In-hospital outcome was change in body weight at 24 hours after randomization; outpatient outcome was worsening heart failure (defined as death, hospitalization, or unscheduled visits for heart failure) at 60 days after randomization.Median (interquartile range) body weight at 24 hours after randomization decreased by -1.80 (-3.85 to -0.50), -2.10 (-3.10 to -0.85), -2.05 (-2.80 to -0.60), and -0.60 (-1.60 to 0.00) kg in the groups receiving tolvaptan 30, 60, and 90 mg/d, and placebo, respectively (Por =.008 for all tolvaptan groups vs placebo). The decrease in body weight with tolvaptan was not associated with changes in heart rate or blood pressure, nor did it result in hypokalemia or worsening renal function. There were no differences in worsening heart failure at 60 days between the tolvaptan and placebo groups (P =.88 for trend). In post hoc analysis, 60-day mortality was lower in tolvaptan-treated patients with renal dysfunction or severe systemic congestion.Tolvaptan administered in addition to standard therapy may hold promise for management of systemic congestion in patients hospitalized for heart failure.

Effects of exercise on dynamic aspects of sleep have not been studied. We hypothesized exercise altered dynamic sleep morphology differently for healthy controls relative to chronic fatigue syndrome (CFS) patients. Sixteen controls (38 ± 9 years) and 17 CFS patients (41 ± 8 years) underwent polysomnography on baseline nights and nights after maximal exercise testing. We calculated transition probabilities and rates (as a measure of relative and temporal transition frequency, respectively) between sleep stages and cumulative duration distributions (as a measure of continuity) of each sleep stage and sleep as a whole. After exercise, controls showed a significantly greater probability of transition from N1 to N2 and a lower rate of transition from N1 to wake than at baseline; CFS showed a significantly greater probability of transition from N2 to N3 and a lower rate of transition from N2 to N1. These findings suggest improved quality of sleep after exercise. After exercise, controls had improved sleep continuity, whereas CFS had less continuous N1 and more continuous rapid eye movement (REM) sleep. However, CFS had a significantly greater probability and rate of transition from REM to wake than controls. Probability of transition from REM to wake correlated significantly with increases in subjective fatigue, pain, and sleepiness overnight in CFS – suggesting these transitions may relate to patient complaints of unrefreshing sleep. Thus, exercise promoted transitions to deeper sleep stages and inhibited transitions to lighter sleep stages for controls and CFS, but CFS also reported increased fatigue and continued to have REM sleep disruption. This dissociation suggests possible mechanistic pathways for the underlying pathology of CFS.