Modern mapping and ablation of idiopathic outflow tract ventricular arrhythmias

Outflow tract (OT) premature ventricular complexes (PVCs) are being recognized as a common and often troubling, clinical electrocardiographic finding. The OT areas consist of the Right Ventricular Outflow Tract (RVOT), the Left Ventricular Outflow Tract (LVOT), the Aortomitral Continuity (AMC), the aortic cusps and the Left Ventricular (LV) summit. By definition, all OT PVCs will exhibit an inferior QRS axis, defined as positive net forces in leads II, III and aVF. Activation mapping using the contemporary 3D mapping systems followed by pace mapping is the cornerstone strategy of every ablation procedure in these patients. In this mini review we discuss in brief all the modern mapping and ablation modalities for successful elimination of OT PVCs, along with the potential advantages and disadvantages of each ablation technique

Η προκαλσιτονίνη και η ιντερλευκίνη-6 ως δείκτες φλεγμονώδους εξεργασίας στο οξύ έμφραγμα μυοκαρδίου και στο οξύ πνευμονικό οίδημα: η κινητική και προγνωστική σημασία αυτών

Objective:Procalcitonin (PCT) is released in severe bacterial infections, sepsis and in infection independent cases such as major surgery, multiple trauma, cardiogenic shock, burns, resuscitation and after cardiac surgery. The aim of this study was to determine the levels and the kinetics of PCT in AMI and to investigate their possible correlation with the release of IL-6 and CRP. Design-Patients: The study included 100 patients (78 men, 22 women, 63.2 ± 14.8 years) with the diagnosis of AMI at admission (group A). In these patients serum levels of PCT, IL-6, CK-MB,TnI and CRP were measured at admission, at 3,6,12,24,48 and 72 hours and at the 7th day. Also enrolled 30 patients (group B) with the diagnosis of acute pulmonary edema, without acute coronary syndrome . Group B was consisted from 18 men and 12 women (68.4 ± 10.8 years). In these patients serum levels of PCT, IL-6, CK-MB,TnI and CRP were measured at admission, immediately after clinical improvement of patients and at the 3rd day. Results: PCT was elevated in all patients with AMI . It was initially detected in serum approximately 2-3 hours after the onset of the symptoms. The median value at admission was 1.41 ng/ml (95% CI: 0.85 to 1.84). The value of PCT showed an increase and reached a plateau after 12-24 hours. The median value at 24 hours was 3.72 ng/ml (95% CI: 2.78 to 4.64). PCT values fell to baseline ( <0.5 ng/ml ) by the 7th day. PCT was detected in serum earlier than CK-MB or TnI in 93 of the 100 patients . The kinetics of PCT was similar to those of CK-MB and TnI. The maximal values of PCT were positively correlated with the maximal values of IL-6 (r=0.59, p=0.00) and of CRP (r=0.61, p=0.001). The maximal values of IL-6 were positively correlated with max CRP (r=0.38, p=0.042). In patients with acute pulmonary edema, without acute coronary syndrome, wasn’t found elevation of PCT. Conclusions: PCT could be considered as a novel sensitive myocardial index. Its release in AMI is probably due to the inflammatory process that occurs during AMI.Η προκαλσιτονίνη εκκρίνεται σε σοβαρές λοιμώξεις, στη σήψη και σε καταστάσεις ανεξάρτητες λοιμώξεων όπως μεγάλες εγχειρήσεις, πολλαπλά τραύματα, καρδιογενή καταπληξία, εγκαύματα, καρδιοαναπνευστική αναζωογόνηση και μετά καρδιοχειρουργική επέμβαση. Σκοπός της προοπτικής αυτής μελέτης ήταν να καθοριστούν τα επίπεδα στο αίμα και η κινητική της προκαλσιτονίνης σε ασθενείς με οξύ έμφραγμα μυοκαρδίου (ΟΕΜ) και σε ασθενείς με οξύ πνευμονικό οίδημα (ΟΠΟ) καρδιακής αιτιολογίας, μη οφειλόμενο σε οξύ στεφανιαίο επεισόδιο. Ακόμη θα διερευνείτο η πιθανή συσχέτιση των επιπέδων της προκαλσιτονίνης με τις αντίστοιχες τιμές της ιντερλευκίνης-6 (IL-6) και της C-αντιδρώσας πρωτείνης (CRP), παράγοντες που έχουν διερευνηθεί και καταδεικνύουν την παρουσία φλεγμονώδους αντίδρασης στα οξέα στεφανιαία σύνδρομα. Η μελέτη συμπεριέλαβε εκατό (100) ασθενείς με τη διάγνωση του οξέος εμφράγματος του μυοκαρδίου κατά την εισαγωγή και τριάντα (30) ασθενείς με τη διάγνωση του οξέος πνευμονικού οιδήματος μη οφειλομένου σε οξύ στεφανιαίο σύνδρομο. Η μέση ηλικία των ασθενών, για την ομάδα με οξύ έμφραγμα μυοκαρδίου, ήταν 63,2±14,8 έτη (78 άνδρες και 22 γυναίκες) και για την ομάδα με οξύ πνευμονικό οίδημα 68,4±10,8 έτη ( 18 άνδρες και 12 γυναίκες ) Στους ασθενείς της ομάδας του ΟΕΜ ελήφθησαν δείγματα αίματος κατά την εισαγωγή στα εξωτερικά ιατρεία και 3,6,12,24,48,72 ώρες αργότερα καθώς και την έβδομη ημέρα. Σε κάθε δείγμα έγινε προσδιορισμός της προκαλσιτονίνης, της ιντερλευκίνης-6, του ισοενζύμου CK-MB, της τροπονίνης Ι και της CRP. Στους ασθενείς της ομάδας του ΟΠΟ ελήφθησαν δείγματα αίματος για τον προσδιορισμό της προκαλσιτονίνης, της IL-6, του ισοενζύμου CK-MB, της τροπονίνης Ι και της CRP κατά την εισαγωγή στο νοσοκομείο, αμέσως μετά την κλινική βελτίωση και τρία εικοσιτετράωρα αργότερα. Η προκαλσιτονίνη αυξήθηκε σε όλους τους ασθενείς με ΟΕΜ. Ανιχνεύθηκε στο αίμα των ασθενών 2-3 ώρες από την έναρξη των συμπτωμάτων. Η ενδιάμεση τιμή της προκαλσιτονίνης στα δείγματα που ελήφθησαν κατά την εισαγωγή ήταν 1,41 ng/ml (με 95% όρια εμπιστοσύνης: 0,85 έως 1,84). Οι τιμές της προκαλσιτονίνης παρουσίασαν οροπέδιο στις 12-24 ώρες. Η ενδιάμεση τιμή της στα δείγματα που ελήφθησαν στις 24 ώρες ήταν 3,72 ng/ml (με 95% όρια εμπιστοσύνης: 2,78 έως 4,64). Τα επίπεδα της προκαλσιτονίνης μειώθηκαν σε τιμές <0,5 ng/ml μέχρι την 7η ημέρα.. Η προκαλσιτονίνη ανιχνεύθηκε στο αίμα νωρίτερα από το ισοένζυμο CK-MB σε 93 από τους 100 ασθενείς. Η κινητική της ήταν παρόμοια με αυτή του ισοενζύμου CK-MB και της τροπονίνης I. Οι υψηλότερες τιμές της προκαλσιτονίνης είχαν θετική συσχέτιση με τις μέγιστες τιμές της ιντερλευκίνης-6 (r=0,59, p=0.000) και της C- αντιδρώσας πρωτείνης (r=0,61, p=0,001). Οι μέγιστες τιμές της ιντερλευκίνης-6 είχαν θετική συσχέτιση με τις μέγιστες τιμές της CRP (r=0,38, p=0,042). Στους ασθενείς με ΟΠΟ, που δεν οφειλόταν σε οξύ στεφανιαίο σύνδρομο, ουσιαστικά δεν παρατηρήθηκε αύξηση της τιμής της προκαλσιτονίνης.. Συμπερασματικά, στη μελέτη αυτή, για πρώτη φορά καταδεικνύεται ο ρόλος της προκαλσιτονίνης στο ΟΕΜ. Με βάση τα δεδομένα μας πρόκειται πιθανώς για ένα δείκτη με ιδιαίτερα υψηλή ευαισθησία και πιθανώς χαμηλή ειδικότητα, που έχει επίσης τη δυνατότητα πρόβλεψης της κλινικής βαρύτητας του οξέος εμφράγματος του μυοκαρδίου

Radial artery as a graft for coronary artery bypass surgery in the era of transradial catheterization

Radial artery use as a bypass conduit is well established during the past decades, in terms of both patency and safety. On the other hand, transradial catheterization causes a series of structural and functional changes to the vessel itself. Impairment of nitric oxide-dependent vasodilation and notable decrease in radial artery diameter due to intima thickening and hyperplasia, especially during the first 3 months after its cannulation, constitute some of the most important alterations on the radial artery wall and its function after a transradial coronary catheterization procedure. Given the constantly increasing numbers of these transradial catheterization procedures, the authors of this article focus on the current knowledge regarding the potential use of the radial artery as a bypass conduit, after its catheterization, also considering several possible mechanisms on its subsequent structural and functional changes. Keywords: Radial artery, Transradial catheterization, Bypass condui

Serum Levels of Gelatinase Associated Lipocalin as Indicator of the Inflammatory Status in Coronary Artery Disease

Background. Atherosclerosis is a chronic inflammatory disease and the acute clinical manifestations represent acute on chronic inflammation. Neutrophil gelatinase-associated lipocalin (NGAL) is found in the granules of human neutrophils, with many diverse functions. The aim of this study was to evaluate the hypothesis that levels NGAL in blood may reflect the inflammatory process in various stages of coronary artery disease. Methods. We studied 140 patients, with SA 40, UA 35, NSTEMI 40, and STEMI 25, and 20 healthy controls. Serum NGAL was measured upon admission and before coronary angiography. Results. Significant differences were observed in median serum-NGAL(ng/mL) between patients with SA (79.23 (IQR, 37.50–100.32)), when compared with UA (108.00 (68.34–177.59)), NSTEMI (166.49 (109.24–247.20)), and STEMI (178.63 (111.18–305.92)) patients and controls (50.31 (44.30–69.78)) with significant incremental value from SA to STEMI. We observed a positive and significant correlation between serum-NGAL and hs-CRP (spearman coefficient rho = 0.685, <0.0001) as well as with neutrophil counts (r = 0.511, <0.0001). Conclusions. In patients with coronary artery disease serum levels of NGAL increase and reflect the degree of inflammatory process. In patients with acute coronary syndromes, serum levels of NGAL have high negative predictive value and reflecting the inflammatory status could show the severity of coronary clinical syndrome

Acute right ventricular myocardial infarction

Acute right ventricular myocardial infarction (RVMI) is observed in 30-50% of patients presenting with inferior wall myocardial infarction (MI) and, occasionally, with anterior wall MI. The clinical consequences vary from no hemodynamic compromise to severe hypotension and cardiogenic shock depending on the extent of RV ischemia. Areas covered: The pathophysiological mechanisms, diagnostic steps, and novel therapeutic approaches of acute RVMI are described. Expert commentary: Diagnosis of acute RVMI is based on physical examination, cardiac biomarkers, electrocardiography, and coronary angiography, whereas noninvasive imaging modalities (echocardiography, cardiac magnetic resonance imaging) play a complementary role. Early revascularization, percutaneous or pharmacological, represents key step in the management of RMVI. Maintenance of reasonable heart rate and atrioventricular synchrony is essential to sustain adequate cardiac output in these patients. When conventional treatment is not successful, mechanical circulatory support, including right ventricle assist devices, percutaneous cardiopulmonary support, and intra-aortic balloon pump, might be considered. The prognosis associated with RVMI is worse in the short term, compared to non-RVMI, but those patients who survive hospitalization have a relatively good long-term prognosis

Acute right ventricular myocardial infarction

Acute right ventricular myocardial infarction (RVMI) is observed in 30-50% of patients presenting with inferior wall myocardial infarction (MI) and, occasionally, with anterior wall MI. The clinical consequences vary from no hemodynamic compromise to severe hypotension and cardiogenic shock depending on the extent of RV ischemia. Areas covered: The pathophysiological mechanisms, diagnostic steps, and novel therapeutic approaches of acute RVMI are described. Expert commentary: Diagnosis of acute RVMI is based on physical examination, cardiac biomarkers, electrocardiography, and coronary angiography, whereas noninvasive imaging modalities (echocardiography, cardiac magnetic resonance imaging) play a complementary role. Early revascularization, percutaneous or pharmacological, represents key step in the management of RMVI. Maintenance of reasonable heart rate and atrioventricular synchrony is essential to sustain adequate cardiac output in these patients. When conventional treatment is not successful, mechanical circulatory support, including right ventricle assist devices, percutaneous cardiopulmonary support, and intra-aortic balloon pump, might be considered. The prognosis associated with RVMI is worse in the short term, compared to non-RVMI, but those patients who survive hospitalization have a relatively good long-term prognosis

Cardiac biomarkers predict 1-year mortality in elderly patients undergoing hip fracture surgery

This prospective study included 152 elderly patients (mean age, 80 years; range, 72-88 years) with a hip fracture treated surgically. Comorbidities were evaluated, and B-type natriuretic peptide was measured at baseline and at postoperative days 4 and 5 in addition to troponin I. Major cardiac events were recorded, and 1-year mortality was assessed. Comorbidity models with the important multivariate predictors of 1-year mortality were analyzed. Overall, 9 patients (6%) experienced major cardiac events postoperatively during their hospitalization. Three patients (2%) died postoperatively, at days 5, 7, and 10, from autopsy-confirmed myocardial infarction. Three patients (2%) experienced a nonfatal myocardial infarction, and 3 patients (2%) experienced acute heart failure. At 1-year follow-up, 37 patients (24%) had died. Age older than 80 years (P=.000), renal failure (P=.016), cardiovascular disease (P=.003), respiratory disease (P=.010), Parkinson disease (P=.024), and dementia (P=.000) were univariate predictors of 1-year mortality. However, in the multivariate model, only age older than 80 years (P=.000) and dementia (P=.024) were important predictors of 1-year mortality. In all comorbidity models, age older than 80 years and dementia were important predictors of 1-year mortality. Postoperative increase in B-type natriuretic peptide was the most important predictor of 1-year mortality. Receiver operating characteristic curve analysis showed a threshold of 90 ng/mL of preoperative B-type natriuretic peptide (area under the curve=0.773, 95% confidence interval, 0.691-0.855, P<.001) had 82% sensitivity and 62% specificity to predict 1-year mortality. Similarly, a threshold of 190 ng/mL of postoperative B-type natriuretic peptide (area under the curve=0.753, 95% confidence interval, 0.662-0.844, P<.001) had 70% sensitivity and 77% specificity to predict the study endpoint

Twenty-Four-Hour Urine (1)-Microglobulin as a Marker of Hypertension-Induced Renal Impairment and Its Response on Different Blood Pressure-Lowering Drugs

The purpose of this study was to assess the role of urine (1)-microglobulin as a marker of hypertension-induced renal damage compared with estimated glomerular filtration rate, (eGFR), urine albumin, and urine albumin-to-creatinine ratio (ACR). Its response on different blood pressure (BP)-lowering drugs was also studied. Sixty never-treated hypertensive patients (65.0% men, 46.9 years, BP 141.4/94.0 mm Hg) were randomized to an irbesartan (an angiotensin receptor blocker [ARB]) or a diltiazem (a nondihydropyridine calcium channel blocker [CCB])-based regimen. Patients with diabetes or established cardiovascular, renal, or liver disease were excluded. Blood samples and 24-hour urine were analyzed at baseline and 6 months after pharmaceutical BP normalization. Serum creatinine was measured and eGFR was calculated. Urine albumin, creatinine, and (1)-microglobulin were measured and ACR was calculated. Minor changes (P=not significant [NS]) in eGFR were noted during follow-up in both groups (from 111.0 mL/min/1.73 m(2) to 108.4 mL/min/1.73 m(2) in the ARB group and from 111.3 mL/min/1.73 m(2) to 114.0 mL/min/1.73 m(2) in the CCB group). Twenty-four-hour urine indices were all significantly improved (P&lt;.01) in the ARB group (albumin from 19.4 mg/L to 8.2 mg/L, ACR from 21.5 mg/g to 10.0 mg/g, (1)-microglobulin from 5.06 mg/L to 3.64 mg/L) but not (P=NS) in the CCB group (albumin from 15.6 mg/L to 13.9 mg/L, ACR from 17.6 mg/g to 17.1 mg/g, (1)-microglobulin from 4.94 mg/L to 4.79 mg/L). These differences between groups remained significant (P&lt;.05) after adjusting for office heart rate and BP. (1)-Microglobulin was significantly correlated (P&lt;.05) with albumin and ACR both at baseline (r=0.283 and 0.299, respectively) and at the end of follow-up (r=0.432 and 0.465, respectively) but not (P=NS) with eGFR. It was also significantly related (P&lt;.05) to cardiovascular risk scores (Framingham and HeartScore) both at baseline (r=0.264 and 0.436, respectively) and at the end of follow-up (r=0.308 and 0.472, respectively). Urine (1)-microglobulin emerges as a potentially usable marker of hypertension-induced renal impairment. Its excretion rate and its response to treatment appears similar to that of albumin. Irbesartan but not diltiazem seems to be associated with reduced excretion of alpha(1)-microglobulin in urine. (C) 2016 Wiley Periodicals, Inc