Confounding factors leading to misdiagnosing ventricular tachycardia as supraventricular in the emergency room.

Studies conducted during the last 50 years have proposed electrocardiographic criteria and algorithms to determine if a wide QRS tachycardia is ventricular or supraventricular in origin. Sustained ventricular tachycardia is an uncommon reason for consultation in the emergency room. The latter and the complexity of available electrocardiographic diagnostic criteria and algorithms result in frequent misdiagnoses. Good hemodynamic tolerance of tachycardia in the supine position does not exclude its ventricular origin. Although rare, ventricular tachycardia in patients with and without structural heart disease may show a QRS duration <120 ms. Interruption of tachycardia by coughing, carotid sinus massage, Valsalva maneuver, or following the infusion of adenosine or verapamil should not discard the ventricular origin of the arrhythmia. In patients with regular, uniform, sustained broad QRS tachycardia, the presence of structural heart disease or A-V dissociation strongly suggest its ventricular origin. Occasionally, ventricular tachycardia can present with AV dissociation without this being evident on the 12-lead ECG. Cardiac auscultation, examination of the jugular venous pulse, and arterial pulse palpation provide additional clues for identifying A-V dissociation during tachycardia. This paper does not review the electrocardiographic criteria for categorizing tachycardia as ventricular but rather why emergency physicians misdiagnose these patients.

N-Terminal Pro-Brain Natriuretic Peptide Is Associated with a Future Diagnosis of Cancer in Patients with Coronary Artery Disease.

OBJECTIVE: Several papers have reported elevated plasma levels of natriuretic peptides in patients with a previous diagnosis of cancer. We have explored whether N-terminal pro-brain natriuretic peptide (NT-proBNP) plasma levels predict a future diagnosis of cancer in patients with coronary artery disease (CAD). METHODS: We studied 699 patients with CAD free of cancer. At baseline, NT-proBNP, galectin-3, monocyte chemoattractant protein-1, soluble tumor necrosis factor-like weak inducer of apoptosis, high-sensitivity C-reactive protein, and high-sensitivity cardiac troponin I plasma levels were assessed. The primary outcome was new cancer diagnosis. The secondary outcome was cancer diagnosis, heart failure requiring hospitalization, or death. RESULTS: After 2.15±0.98 years of follow-up, 24 patients developed cancer. They were older (68.5 [61.5, 75.8] vs 60.0 [52.0, 72.0] years; p=0.011), had higher NT-proBNP (302.0 [134.8, 919.8] vs 165.5 [87.4, 407.5] pg/ml; p=0.040) and high-sensitivity C-reactive protein (3.27 [1.33, 5.94] vs 1.92 [0.83, 4.00] mg/L; p=0.030), and lower triglyceride (92.5 [70.5, 132.8] vs 112.0 [82.0, 157.0] mg/dl; p=0.044) plasma levels than those without cancer. NT-proBNP (Hazard Ratio [HR]=1.030; 95% Confidence Interval [CI]=1.008-1.053; p=0.007) and triglyceride levels (HR=0.987; 95%CI=0.975-0.998; p=0.024) were independent predictors of a new cancer diagnosis (multivariate Cox regression analysis). When patients in whom the suspicion of cancer appeared in the first one-hundred days after blood extraction were excluded, NT-proBNP was the only predictor of cancer (HR=1.061; 95%CI=1.034-1.088; p<0.001). NT-proBNP was an independent predictor of cancer, heart failure, or death (HR=1.038; 95%CI=1.023-1.052; p<0.001) along with age, and use of insulin and acenocumarol. CONCLUSIONS: NT-proBNP is an independent predictor of malignancies in patients with CAD. New studies in large populations are needed to confirm these findings.

Usefulness of a combination of monocyte chemoattractant protein-1, galectin-3, and N-terminal probrain natriuretic peptide to predict cardiovascular events in patients with coronary artery disease.

Patients with coronary artery disease may develop not only ischemic events but also heart failure and death due to previous myocardial damage. The purpose of this study was to test the prognostic value of a panel of plasma biomarkers related to vascular (monocyte chemoattractant protein-1 [MCP-1] and soluble tumor necrosis factor-like weak inducer of apoptosis) and myocardial damage (galectin-3, N-terminal fragment of brain natriuretic peptide [NT-proBNP], and neutrophil gelatinase-associated lipocalin) in 706 patients with chronic coronary artery disease followed for 2.2 ± 0.99 years. Secondary outcomes were the incidence of acute ischemic events (ST elevation myocardial infarction, non-ST elevation acute coronary syndrome, stroke, or transient ischemic attack) and death or heart failure. The primary outcome was the combination of the secondary outcomes. Cox proportional hazards model was used for analysis. Fifty-three patients developed acute ischemic events. Increasing MCP-1 plasma levels (p = 0.002), age, and body mass index predicted this outcome independently. Thirty-three patients developed death and/or heart failure. Galectin-3 (p = 0.007), NT-proBNP plasma levels (p = 0.004), hypertension, glomerular filtration rate, and the use of nitrates and anticoagulants were associated with this outcome independently. The development of the primary outcome was predicted independently by MCP-1 (p <0.001), NT-proBNP (p = 0.005), and galectin-3 (p = 0.019); hypertension; atrial fibrillation; and treatment with nitrates. Every biomarker with a value above the median increased the risk of developing this outcome by 1.832 (95% confidence interval 1.356 to 2.474, p <0.001). High-sensitivity C-reactive protein and lipid levels were not associated with any outcome. In conclusion, increasing MCP-1, galectin-3, and NT-proBNP plasma levels are associated with a greater incidence of cardiovascular events.

Cardiac anatomy for the interventional arrhythmologist: I.terminology and fluoroscopic projections.

Cardiac anatomy is complex and its understanding is essential for the interventional arrhythmologist. The first difficulty is the terminology used to describe the location of sites of mapping and ablation. For many years, electrophysiologists have named these positions following the conventional electrocardiographical vocabulary, or the terminology used by surgeons performing arrhythmic surgery. This traditional nomenclature, however, failed to take note of the crucial principle of considering the location of the heart in the human body as viewed in its erect position. In other words, it had failed to use an attitudinally appropriate terminology. Almost 10 years ago, a new attitudinal nomenclature was proposed for the right and left atrioventricular junctions. In this first of a series of reviews of cardiac anatomy as seen by the interventional arrhythmologist, we discuss the role of attitudinally appropriate terminology, and relate this to the projections used for cardiac fluoroscopy, fluorography, and angiography. Throughout our series of reviews, we will illustrate the value of The Visible Human Slice and Surface Server in facilitating the understanding of the fluoroscopic anatomy. (PACE 2010; 497-507).

Multicystic/cavitated giant left atrial myxomas: a matter of technology?

We present the case of a rare echocardiographic image of a giant cavitated myxoma and the pathologic findings of the cystic mass. The new echocardiographic equipment not only has improved the sensitivity for diagnosis of different pathologies but also has redefined its visual and morphologic characteristics. Although most myxomas are solid masses and some cystic myxomas have been reported, the presence of multiple cavities on echocardiographic exam has exceptionally been described. While cystic changes have been described at autopsy in 14% of cardiac myxomas, its identification with echocardiography is rare. Nowadays, the new echocardiographic equipment has improved the quality and the accuracy to detect and describe intracardiac masses, showing myxomas with cystic cavities in vivo that in the past was a pathologic finding.

Loeffler endocarditis: what have we learned?

Loeffler endocarditis, eosinophilic endomyocardial disease or fibroplastic endocarditis appears to be a subcategory of the Hypereosinophilic syndrome in which the heart is predominantly involved. It is an uncommon myocardial disease, thought to be secondary to eosinophils damage, characterized by fibrous thickening of the endocardium of one or both ventricles, leading to apical obliteration and multiple cardiovascular complications. Despite all the efforts, the ultimate responsible mechanisms of this entity remain unresolved. Many theories have been raised trying to explain this phenomenon, but nowadays the enigma in relation to the different patterns of evolution continues. In this concise review we discuss the different pathophysiologic theories postulated and the management of the cardiovascular complications. Perhaps it will serve to assist in recognition of patients with the same condition around the world.

Multicavitated left atrial myxoma mimicking a hydatid cyst.

A 67 year-old asymptomatic patient was referred to our echo-lab because of hypertension. Transthoracic 2D-echocardiogram showed a non-prolapsing ovoid mass attached to the left side of the interatrial septum. Transesophageal echocardiography evidenced an ovoid cavitated mass with internal areas of calcification. Color Doppler revealed flow inside the cavities. At surgery, a multicavitated mass was observed attached to interatrial septum. Macroscopically revealed cavities filled with blood, as well as partially calcified areas. Microscopically there were collections of "lipidic" cells embedded in the myxoid matrix, typical of cardiac myxoma. Cardiac hydatid cysts usually have a rounded shape. Most myxomas are solid masses without a cystic architecture or cavitations. Calcification is usually identified at a microscopic level. The combination of a polycystic appearance of the mass and macroscopic areas of calcification is more frequently observed in hydatid cysts than in cardiac myxomas. This appearance of the mass leads us to consider a cardiac echinococcal cyst as the first diagnostic possibility. This peculiar structure of cardiac myxoma, to the best of our knowledge, has never been documented. Transthoracic echocardiography and particularly transesophageal imaging, enable us to delineate this kind of tumors. Surgical resection is the appropriate treatment for these tumors, even in asymptomatic patients.

How close are the phrenic nerves to cardiac structures? Implications for cardiac interventionalists.

BACKGROUND: Phrenic nerve injury is a recognized complication following cardiac intervention or surgery. With increasing use of transcatheter procedures to treat drug-refractory arrhythmias, clarification of the spatial relationships between the phrenic nerves and important cardiac structures is essential to reduce risks. METHODS AND RESULTS: We examined by gross dissection the courses of the right and left phrenic nerves in 19 cadavers. Measurements were made of the minimal and maximal distances of the nerves to the superior caval vein, superior cavoatrial junction, right pulmonary veins, and coronary veins. Histologic studies were carried out on tissues from six cavaders. Tracing the course of the right phrenic nerve revealed its close proximity to the superior caval vein (minimum 0.3 +/- 0.5 mm) and the right superior pulmonary vein (minimum 2.1 +/- 0.4 mm). The anterior wall of the right superior pulmonary vein was <2 mm from the right phrenic nerve in 32% of specimens. The left phrenic nerve passed over the obtuse cardiac margin and the left obtuse marginal vein and artery in 79% of specimens. In the remaining specimens, its course was anterosuperior, passing over the main stem of the left coronary artery or the anterior descending artery and great cardiac vein. CONCLUSIONS: The right phrenic nerve is at risk when ablations are carried out in the superior caval vein and the right superior pulmonary vein. The left phrenic nerve is vulnerable during lead implantation into the great cardiac and left obtuse marginal veins.

Cardiac granulocytic sarcoma (chloroma): in vivo diagnosis with transesophageal echocardiography.

Granulocytic sarcoma, or chloroma, is an uncommon presentation of acute leukemia. Cardiac involvement is very rare and usually diagnosed at autopsy. We present a case that discloses the essential role of transesophageal echocardiography for its in vivo diagnosis. The principal features with this imaging technique are finely described.

Mapping and ablation of ventricular fibrillation associated with long-QT and Brugada syndromes.

BACKGROUND: The long-QT and Brugada syndromes are important substrates of malignant ventricular arrhythmia. The feasibility of mapping and ablation of ventricular arrhythmias in these conditions has not been reported. METHODS AND RESULTS: Seven patients (4 men; age, 38+/-7 years; 4 with long-QT and 3 with Brugada syndrome) with episodes of ventricular fibrillation or polymorphic ventricular tachycardia and frequent isolated or repetitive premature beats were studied. These premature beats were observed to trigger ventricular arrhythmias and were localized by mapping the earliest endocardial activity. In 4 patients, premature beats originated from the peripheral right (1 Brugada) or left (3 long-QT) Purkinje conducting system and were associated with variable Purkinje-to-muscle conduction times (30 to 110 ms). In the remaining 3 patients, premature beats originated from the right ventricular outflow tract, being 25 to 40 ms ahead of the QRS. The accuracy of mapping was confirmed by acute elimination of premature beats after 12+/-6 minutes of radiofrequency applications. During a follow-up of 17+/-17 months using ambulatory monitoring and defibrillator memory interrogation, no patients had recurrence of symptomatic ventricular arrhythmia but 1 had persistent premature beats. CONCLUSIONS: Triggers from the Purkinje arborization or the right ventricular outflow tract have a crucial role in initiating ventricular fibrillation associated with the long-QT and Brugada syndromes. These can be eliminated by focal radiofrequency ablation.