Rhythmos (E-Journal - First Department of Cardiology / Evagelismos General Hospital of Athens)
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Ηλεκτροκαρδιογραφικό Quiz
No full textΤο παρακάτω ΗΚΓ ανήκει σε υγιή γυναίκα 50 ετών. Ποιά η διάγνωσή σας? ... (excerpt
Cardiology News /Recent Literature Review / Second Quarter 2013
Get PDFESC Congress will be held in Amsterdam, 31/8-4/9/13 HCS Meeting: Athens, 10-12/10/2013 TCT Meeting: San Francisco, 28/10-1/11/13 AHA 2013: Dallas, 16-20/11/13 ACC 2014: Washington, DC, 29-31/3/2014 Athens Cardiology Update 2014: Athens (Crown Plaza Hotel), 10-12/4/2014 HRS Meeting: San Francisco, 7-10/5/2014 EuroPCR: Paris, 20-23/5/2014 CardioStim 2014: Nice, 18-21/6/2014 ARMYDA-9 CAROTID: Clopidogrel Load & Atorvastatin Reload Prevent Ischemic Cerebral Events After Protected Carotid StentingA total of 156 patients undergoing protected carotid stenting were randomized to a 600-mg (n=78) or 300-mg (n=78) clopidogrel load given 6 h before intervention and either an atorvastatin reload (n=76; 80 mg + 40 mg initiating 12 h before the procedure) or no statin reload (n=80). Occurrence of the primary outcome (30-day incidence of TIA/stroke or new ischemic lesions on cerebral MRI performed at 24-48 h) was lower in the 600-mg clopidogrel arm (18% vs. 35.9% in the 300-mg group; p = 0.019) and in the atorvastatin reload arm (18.4% vs 35.0% in the no statin reload group; p=0.031). High-dose clopidogrel also significantly reduced the TIA/ stroke rate at 30 days (0% vs 9%, p = 0.02), without an increase in bleeding risk. The authors concluded that in patients undergoing carotid stenting, a 600-mg clopido-grel load and a short-term reload with high-dose atorva-statin protects against early ischemic cerebral events (Patti G et al, J Am Coll Cardiol 2013;61:1379-1387) MADIT CRT: Carvedilol Produces 30% Reduction in Hospitalizations for HF or Death When Compared With MetoprololThe effects of metoprolol and carvedilol were compared in the MADIT-CR study. Hospitalization for HF or death occurred in 23% on carvedilol and 30% on metoprolol (hazard ratio-HR: 0.70, p=0.001), further attenuated in the subgroup of CRT-D patients (HR: 0.61, p = 0.001) and CRT-D patients with LBBB (HR: 0.51, p < 0.001). Ventricular arrhythmias occurred in 22% and in 26%, respectively, of the patients receiving carvedilol or metoprolol (HR: 0.80, p = 0.050). A dose-dependent relationship was found in carvedilol, but not in metoprolol. The authors concluded that in HF patients in NYHA class I/II & wide QRS, carvedilol was associated with a 30% reduction in hospitalizations for HF or death when compared with metoprolol. A novel beneficial and synergistic effect of carvedilol was seen in patients with CRT-D & LBBB. Finally, a dose-dependent effect was apparent in carvedilol, but not in metoprolol (Ruwald et al, J Am Coll Cardiol 2013;61:1518–1526)... (excerpt
Είναι η Κολπική Μαρμαρυγή Φλεγμονώδης Νόσος?
No full textΣε πρόσφατη δημοσίευση, έγινε διερεύνηση 3 δεικτών φλεγμονής, CRP, sICAM (soluble intercellular adhesion molecule), & ινωδογόνου, σε γυναικείο πληθυσμό (ν=24734) της μελέτης Women’s Health Study, που δεν είχε εξ αρχής κολπική μαρμαρυγή (κΜ) (Conen et al, Eur Heart J 2010, online:May 25, 2010). Σε διάρκεια 14.4 ετών, 747 (3%) γυναίκες εμφάνισαν το πρώτο επεισόδιο κΜ. Οι παραπάνω 3 δείκτες φλεγμονής συσχετίζονταν ατομικά και μετά απο διόρθωση για τους κλασικούς παράγοντες κινδύνου, με την εμφάνιση κΜ. Ο κίνδυνος κΜ ήταν ανάλογος του score φλεγμονής, βαθμιαία αυξανόμενος απο 1.66 σε 3.25 συμβάματα ανά 1000 άτομα-έτη απο το χαμηλότερο στο υψηλότερο score φλεγμονής (Εικόνα 1). Όπως τονίζουν οι συγγραφείς, ενώ έχει καταδειχθεί ότι η φλεγμονή μετά απο καρδιακή εγχείρηση μπορεί να οδηγήσει σε μετεγχειρητική κΜ, παραμένει υπο αμφισβήτηση εαν η φλεγμονή παίζει κάποιο ρόλο στην εμφάνιση της κΜ σε άλλες περιπτώσεις. Μαζί με αυτή τη μελέτη, 3 προοπτικές μελέτες κατέδειξαν ότι η CRP άμεσα συνδέεται με την επίπτωση κΜ (Cardiovascular Health Study & μελέτη Framingham), ωστόσο η ταυτόχρονη εξέταση πολλαπλών δεικτών φλεγμονής μπορεί να παράσχει καλύτερη εικόνα της φλεγμονώδους διασύνδεσης με την κΜ. Έτσι, διαφαίνεται ότι η χρόνια φλεγμονή μπορεί να έχει προ-αρρυθμική δράση και να οδηγήσει σε κΜ σε ευαίσθητα άτομα...(excerpt
Οι Νέες Κατευθυντήριες Οδηγίες Ανάνηψης 2010 (Διεθνείς & Αμερικάνικες)
No full textΣε πρόσφατη διπλή δημοσίευση (Circulation 2010;122 (suppl 2):S250 –S275./ Circulation 2010; 122 (suppl 3):S640 –S656) περιελήφθησαν οι νέες κατευθυντήριες οδηγίες ανάνηψης της Διεθνούς Επιτροπής Ανάνηψης (ILCOR) και της Αμερικανικής Καρδιολογικής Εταιρείας (AHA). Σε σύγκριση με τις προηγούμενες οδηγίες του 2005, σημαντικές πρόοδοι και εξελίξεις έχουν επέλθει και διαμείβονται στις νέες οδηγίες. Μια βραχύτατη περίληψη αυτών περιλαμβάνεται παρακάτω. ● Οι κοινοί διασώστες ξεκινούν την ανάνηψη εαν το θύμα δεν απαντά και δεν αναπνέει φυσιολογικά (αγνοώντας κάποιες αγωνιώδεις αναπνοές) χωρίς να ελέγξουν τον σφυγμό. ● Οι διασώστες ξεκινούν την ανάνηψη με καρδιακές μόνον μαλάξεις χωρίς τεχνητή αναπνοή ● Όλοι οι διασώστες (εκπαιδευμένοι και μη) πρέπει να παράσχουν ικανές καρδιακές μαλάξεις στα θύματα καρδιακής ανακοπής με ώσεις σε βάθος συμπίεσης τουλάχιστον 5 cm και συχνότητα τουλάχιστον 100/λεπτό, επιτρέποντας πλήρη επανέκπτυξη του θώρακα μετά απο κάθε μάλαξη και ελαχιστοποιώντας τις διακοπές των μαλάξεων ● Οι εκπαιδευμένοι διασώστες πρέπει να παράσχουν επίσης τεχνητή αναπνοή με αναλογία μαλάξεων-αερισμών 30:2 Επομένως αλλάζει η σειρά ανάνηψης απο ABC (airway-breathing-circulation/αεραγωγός-αναπνοή-κυκλοφορία) σε CAB (circulation-airway-breathing/ κυκλοφορία-αεραγωγός-αναπνοή (όπου κυκλοφορία βλ. μαλάξεις θώρακα). Το σύστημα επείγουσας βοήθειας θα πρέπει να ενεργοποιηθεί άμεσα σε κάθε περίπτωση που ανευρίσκεται άτομο που δεν απαντά. Η ενσωμάτωση των αυτόματων εξωτερικών απινιδωτών (AED) στην Αλυσίδα Επιβίωσης (Chain of Survival) είναι κρίσιμη...(excerpt
Magnetic Resonance Imaging and Implantable Devices
Get PDFIn recent years, there has been a remarkable increase in the number of patients who benefit from cardiovascular implantable devices. On the other hand, magnetic resonance imaging (MRI) compared with other imaging techniques undoubtedly has many advantages regarding its discrimination ability without radiation exposure. The risks of scanning device patients that have non “MR Safe” or “MRConditional” devices (Table 1), due to field effects, are well known as are the risk mitigation strategies. Hazards and safety concerns There are three distinct mechanisms associated with MRI that can give rise to potential risks related to cardiovascular devices: (1) the static magnetic field, (2) radiofrequency (RF) energy, (3) gradient magnetic fields or any combination of them. Static main magnetic field exposes ferromagnetic components to mechanical forces and torque and causes unpredictable magnetic sensor activation, reed switch closure and electrocardiograms distortions on electronic implantable pulse generators (IPGs), implantable cardioverter defibrillators (ICDs) and cardiac resynchronization therapy (CRT) devices. Modulated RF field interacts with pacemaker devices and leads causing heating of cardiac tissue adjacent to electrodes, reset and sensing problems of the device. ICDs can falsely detect RF field as ventricular tachycardia (VT) and start the sequence of defibrillation. Gradient magnetic field can induce currents in electrically conductive wires and leads that could cause over-/under-sensing and induce arrhythmias. Combined field effects can cause alteration of device function, vibrations, electronic reset and device or lead damage. Electrical reset is a safety emergency mode that limits pacemaker functionality to minimal in case of battery depletion or dip due to MR field interference. Factory default settings and usually a VVI mode are set while ICD therapies are deactivated. Because ICD’s parts, such as capacitors and batteries, are much larger than those of pacemakers and the technology used is more complicated they tend to pose greater conflicts, electromagnetic and mechanical forces (10 times higher than pacemaker), under MRI conditions. Generally pacemakers are switched to asynchronous magnet or interference mode and ICD therapy is switched off after MR field exposure... (excerpt
Evidence Linking Obstructive Sleep Apnea to Hypertension
Get PDFObstructive sleep apnea (OSA) has been linked to hypertension in several experimental, epidemiological, and clinical studies. Animal modes of sleep apnea have provided strong evidence for a causal relationship with hypertension. Studies in humans have demonstrated that patients with sleep apnea have an increased blood pressure and a higher incidence of hypertension. The most compelling evidence linking OSA and hypertension was provided by data from the Wisconsin Sleep Cohort Study. This study has demonstrated a dose-response association between sleep-disordered breathing at baseline and the presence of de novo hypertension 4 years later. The odds ratios for the presence of hypertension at the 4-year follow-up study according to the apnea-hypopnea index (AHI) at base line were estimated after adjustment for baseline hypertension status, body mass index (BMI), neck and waist circumference, age, gender, and weekly use of alcohol and tobacco. Relative to the reference category of an AHI of 0 events per hour at baseline, the odds ratios for the presence of hypertension at follow-up were 1.42 (95% confidence intervals-CI 1.13-1.78) with an AHI of 0.1-4.9 events per hour at base line as compared with none, 2.03 (95% CI 1.29-3.17) with an AHI of 5.0-14.9 events per hour, and 2.89 (95% CI 1.46-5.64) with an AHI of 15.0 or more events per hour. These findings suggest two important concepts. First, sleep-disordered breathing is a risk factor for hypertension in the general population. Second, even sleep apnea that is considered mild may also contribute significantly to overall blood pressure levels...(excerpt
Recent Data on Epicardial Ablation of Ventricular Tachycardia in Nonischemic Heart Disease
Get PDFEpicardial ablation has been adopted during the last years, mainly as a supplementary technique after a failed endocardial ablation procedure, both in patients with ischemic and nonischemic ventricular tachycardias (VTs). Sosa and colleagues were the first who described the percutaneous subxiphoidal puncture to approach the epicardial space in 1996. Using the 3D electroanatomic mapping systems, the endocardial and epicardial substrate mapping have become feasible during the same procedure. Because of its complexity and its potential risks this process is performed only in high experienced centers by skilled operators with a large number of VT ablation procedures.Endocardial ablation in patients with left ventricular nonischemic cardiomyopathy (NICM) has shown worst outcome compared with ablation in ischemic cardiomyopathy. The main reason seems to be the progressive nature of the disease and the presence of epicardial and intramural slow conduction areas forming reentry circuits. The pattern of fibrosis and scar in NICM is not predictable as in ischemic cardiomyopathy where it follows the distribution of the coronary artery disease. Data from the study of Hsia et al in patients with NICM and VT episodes supported that the critical endocardial low voltage substrate was located mainly in the basal and perivalvular area. In this study, epicardial mapping was performed only in few patients revealing abnormal fragmented potentials but data from later studies highlighted the important of epicardial substrate in NICM. Cano et al3 performed both endocardial and epicardial mapping in 22 patients either because of failed endocardial ablation or because of electrocardiographic signs suggesting epicardial localization of the exit point. Electroanatomic mapping revealed extended epicardial low voltage areas in the majority of the patients (about 82%) which were located mostly in basal left ventricular lateral wall. However, Haqqani et al described 31 of 266 patients with NICM (11.6%) who had septal involvement, mainly in the basal region, without lateral low voltage areas... (excerpt
Device Therapy in Refractory Heart Failure
Get PDFAdvanced heart failure (HF) has been defined as persistent symptoms that limit daily life despite optical medical therapy, corresponding to New York Heart Association (NYHA) class III/IV symptoms or to the newer classification of stage D HF (ACC/AHA staging classification). It affects 10% of the HF population and is associated with a poor quality of life, recurrent hospitalizations and a mortality approaching 50% at 1 year and 80% at 5 years. Despite the widespread use of angiotensin converting enzyme (ACE) inhibitors, beta adrenergic blocking agents and spironolactone which improve the prognosis in mild to moderate stages, HF remains a progressive disease leading to decompensation and demand of both inotropic agents (class III recommendation according to ACC/AHA guidelines, considered solely for palliation in patients with end-stage disease) and diuretics to treat hypotension, impaired renal function and pulmonary congestion.Heart transplantation (HT) is associated with nearly 90% 1-year survival, 60% 10-year survival and 95% freedom from symptoms and activity limitations in survivors throughout the follow-up period. Nevertheless, the lack of available donors and the large number of patients, who do not meet the criteria for transplantation, have spurred interest in cardiac resynchronization therapy (CRT) and mechanical circulatory support (MCS), providing alternatives for patients waiting for HT (bridge to transplantation, BTT), patients who are ineligible for HT (destination therapy, DT) or patients who are anticipated to recover after left ventricular unloading (bridge to recovery, BTR)... (excerpt
Leadless Pacing: The Future is not Here Yet!
Get PDFDespite great technical advances over the last decades, cardiac pacing is still associated with a significant rate of complications mostly ascribed to the pacing leads. Leads are susceptible to mechanical stress, whether transvenous or epicardial, and constitute the pacing component most prone to failure; they are the major contributor to compli-cations, may cause vascular obstruction, and other late complications, such as mechanical failure and infection, whereby extraction is required with its attendant dire consequences. Implantation of a pacemaker in young patients exposes them to high risk of subsequent lead complications, and when failed leads are replaced without extraction, the presence of multiple endocardial leads may cause major vascular morbidity. New devices for bi-ventricular or bifocal pacing to effect cardiac resynchro-nization therapy (CRT) incorporating 3 leads are associa-ted with even more problems. Hence, there came about a resurge of interest in the technology of leadless pacing.The first totally self-contained leadless pacemaker system was proposed by Spickler back n 1970 using a device powered by mercury-zinc and nuclear power that was successfully tested in animals. Almost 30 years later, Gotto et al tested an automatic power-generating system (AGS) which converts kinetic into electric energy for quartz watches as a power source for cardiac pacemakers. They could demonstrate that the circuit generated pulses of 0.5 ms width at 1 Hz (60 pulses/min). The voltage of the AGS was maintained at 1.6 V while it was being charged by the accelerations. The generator supplied pulses of 0.75 V, 1.47 mA via a 510-ohm load. With fully charged AGS, the generator was also used to pace a mongrel dog\u27s heart at 140 beats/min for 60 min. During pacing, the AGS supplied 420 mJ to the circuit and the cardiac muscle. The AGS was placed on the right ventricular wall of the dog under anesthesia. Energy of 80 mJ is stored in a capacitor by the heart beating at ~ 200 beats/min for 30 min. Thus, the AGS generated 13 microJ per heart beat. This result suggested that the AGS could supply enough energy for use in a cardiac pacemaker... (excerpt
Cardiology News /Recent Literature Review / First Quarter 2013
Get PDFHRS Meeting will take place in Denver, 8-11/5/13 EuroPCR to be held in Paris, 21-24/5/13 EuroPace will be held in Athens, 23-26/6/13 ESC Congress will be held in Amsterdam, 31/8-4/9/13 TCT Meeting: San Francisco, 28/10-1/11/13 AHA 2013: Dallas, 16-20/11/13 Pre-RELAX-AHF and RELAX-AHF Trials: Relaxin Reduces 6-month Mortality in Acute Heart Failure Patients In the Pre-RELAX-AHF (Relaxin in Acute Heart Failure) phase II study and RELAX-AHF phase III study patients hospitalized for acute heart failure were randomized within 16 h to IV placebo or serelaxin. Serelaxin reduced 6-month mortality in both studies (combined studies: N = 1,395; hazard ratio: 0.62; p = 0.0076). In RELAX-AHF, serelaxin improved the markers of cardiac (high-sensitivity cardiac troponin T), renal (creatinine/cystatin-C), and hepatic (AST/ALT) damage and of decongestion (N-T pro–BNP), while changes in these markers at day 2 and worsening heart failure during admission were associated with 6-month mortality. The authors concluded that early administration of serelaxin was associated with a reduction of 6-month mortality, while fewer signs of organ damage and more rapid relief of congestion were noted during the first days after admission (Metra et al, J Am Coll Cardiol 2013;61:196–206) Favorable 5-Year Outcome after TAVI The 5-year outcome was evaluated in 88 patients undergoing successful TAVI with a balloon-expandable valve. Mean aortic valve gradient decreased from 46 + 18 mm Hg to 10 + 4.5 mm Hg after TAVI and maintained at 11.8 + 5.7 mm Hg at 5 years (p for post-TAVI trend = 0.06). Mean aortic valve area increased from 0.62 + 0.17 cm2 to 1.67 + 0.41 cm2 after TAVI and 1.40 + 0.25 cm2 at 5 years (p for post-TAVI trend <0.01). At 5 years, 3 patients (3.4%) had moderate prosthetic valve dysfunction. Survival rates at 1 to 5 years were 83%, 74%, 53%, 42%, and 35%, respectively. Median survival time after TAVI was 3.4 years, and the risk of death was significantly increased in patients with chronic obstructive pulmonary disease (hazard ratio [HR]: 2.17) and at least moderate paravalvular regurgitation (adjusted HR: 2.98). Thus, a favorable long-term outcome after TAVI was demonstrated. Signs of moderate prosthetic valve failure were observed in 3.4% of patients. No patients developed severe prosthetic regurgitation or stenosis. Comorbidities, mainly chronic lung disease and at least moderate paravalvular regurgitation, were associated with reduced long-term survival (Toggweiler et al, J Am Coll Cardiol 2013;61:413–419)... (excerpt