10ο Πανελλήνιο Συνέδριο Καρδιακής Ανεπάρκειας

Από Παρασκευή, 6. Φεβρουάριος 2009
Πρός Κυριακή, 8. Φεβρουάριος 2009

Τοποθεσία: Ξενοδοχείο "Divani Caravel", Αθήνα
Επαφή: Εταιρεία Μελέτης και Έρευνας της Καρδιακής Ανεπάρκειας (Ε.Μ.Ε.Κ.Α.)
e-mail: mailemeka@gmail.com

ΚΑΤΑΛΗΚΤΙΚΗ ΗΜΕΡΟΜΗΝΙΑ ΥΠΟΒΟΛΗΣ ΕΡΓΑΣΙΩΝ: 10 ΙΑΝΟΥΑΡΙΟΥ 2009


Οι περιλήψεις υποβάλλονται μόνο ηλεκτρονικά ως επισυναπτόμενο word αρχείο στην ηλεκτρονική διεύθυνση mailemeka@gmail.com

Οδηγίες για την συγγραφή της περίληψης:

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• Ο τίτλος της εργασίας, που δεν θα πρέπει να υπερβαίνει τους 70 χαρακτήρες, να γραφεί με κεφαλαία γράμματα
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• Αφήστε μια σειρά κενή πριν αρχίσετε το κείμενο της περίληψης, το οποίο δεν θα πρέπει να υπερβαίνει τις 250 λέξεις
• Στην περίπτωση που χρησιμοποιηθούν συντομογραφίες, να αναφερθεί την πρώτη φορά ολογράφως
• Μην συμπεριλάβετε γραφικά στο κείμενο της περίληψης
• Τα κείμενα θα συμπεριληφθούν στο Βιβλίο Περιλήψεων όπως ακριβώς υποβλήθηκαν προς έγκριση. Διορθώσεις ή αντικαταστάσεις κειμένων δεν θα γίνουν αποδεκτές από την Επιστημονική Επιτροπή
• Στη συνοδευτική σας επιστολή/μήνυμα πρέπει να αναφέρετε απαραιτήτως τον τρόπο που επιθυμείτε να παρουσιάσετε την εργασία σας (προφορική ή αναρτημένη ανακοίνωση) καθώς και προσωπικά στοιχεία (ονοματεπώνυμο, ταχυδρομική δ/νση, τηλέφωνο, e-mail) του υπευθύνου συγγραφέα για μελλοντική ενημέρωση σχετικά με την εργασία
• Η Επιστημονική Επιτροπή διατηρεί το δικαίωμα της τελικής απόφασης για τον τρόπο παρουσίασης της εργασίας
• Η εγγραφή στο συνέδριο τουλάχιστον ενός εκ των συγγραφέων είναι απαραίτητη για να γίνει αποδεκτή η παρουσίαση της εργασίας
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13-14/12/2008, 4-5/04/2009

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Journal Club 2/10/2008

Episodic syncope in hypertrophic cardiomyopathy: evidence for inappropriate vasodilation
K Prasad, L Williams, R Campbell, P M Elliott, W J McKenna and M Frenneaux

Heart 2008;94;1312-1317; Originally published online 24 Jul 2008; doi:10.1136/hrt.2008.141507

Symptoms of impaired consciousness (syncope and presyncope)
occur in 15–25% of patients with hypertrophic cardiomyopathy (HCM). In young patients a history of recurrent syncope is associated with an increased risk of sudden death.

Syncope usually occurs without warning or symptoms suggestive of the cause. Detailed investigations identify a probable mechanism in a minority, usually paroxysmal atrial fibrillation or ventricular tachycardia. In the majority however no likely mechanism is found despite repeated 24-hour ambulatory echocardiography (ECG) or patient-activated monitoring, exercise testing and invasive electrophysiological studies.

Empirical treatment with amiodarone, a pacemaker or an implantable cardioverter-defibrillator is commonly employed, but is often unsuccessful in relieving the symptoms.
We have previously observed that approximately 30% of patients with HCM have abnormal blood pressure response during maximal upright exercise.
This was due in the majority of patients to an exaggerated fall in systemic vascular resistance, possibly arising from abnormal activation of stretch-sensitive left ventricular mechanoreceptors, by a mechanism similar to that described in aortic stenosis.
However, in some patients an inadequate cardiac output response to exercise may be responsible. We hypothesised that abnormal vasodepressor-mediated hypotension may also occur during daily life in patients with HCM, and that this may
be an important mechanism of syncope when conventional
investigations fail to reveal a cause.
CONCLUSIONS
Episodic hypotension occurs during ordinary activity in HCM patients with symptoms of impaired consciousness and is associated with abnormal blood pressure responses during maximal exercise.
This hypotension was due to inappropriate vasodilation. Our data suggest that these episodes may be an important cause of syncope in HCM
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Abnormal papillary muscle morphology is
independently associated with increased left ventricular outflow tract obstruction in
hypertrophic cardiomyopathy

D H Kwon, R M Setser, M Thamilarasan, Z V Popovic, N G Smedira, P Schoenhagen, M J Garcia, H M Lever and M Y Desai

Heart 2008;94;1295-1301; originally published online 9 Aug 2007; doi:10.1136/hrt.2007.118018
Background: Abnormal papillary muscles (PM) are often found in hypertrophic cardiomyopathy (HCM).
Objective: To assess the relationship between morphological alterations of PM in patients with HCM and left ventricular outflow tract (LVOT) obstruction, using magnetic resonance imaging (MRI) and echocardiography.
Methods: Fifty-six patients with HCM (mean age 42 years (interquartile range 27, 51), 70% male) and 30 controls (mean age (42 (30, 53) years, 80% male) underwent MRI on a 1.5 T scanner (Siemens, Erlangen, Germany). Standard cine images were obtained in shortaxis (base to apex), along with two-, three- and fourchamber views. The presence of bifid PM (none, one or both) and anteroapical displacement of anterolateral PM was recorded by MRI and correlated with resting LVOT gradients obtained by echocardiography.
Results: Double bifid PM (70% vs 17%) and anteroapical displacement of anterolateral PM (77% vs 17%) were more prevalent in patients with HCM than in controls (p,0.001).
Subjects with anteroapically displaced PM and double bifid PM had higher resting LVOT gradients than controls (45 (6, 81) vs 12 (0, 12) mm Hg (p,0.01) and 42 (6, 64) vs 11 (0, 17) mm Hg (p=0.02), respectively. In patients with HCM, the odds ratio of having significant (>30 mm Hg) peak resting gradient was 7.1 (95% CI 1.4 to 36.7) for anteroapically displaced anterolateral PM and 10.4 (95% CI 1.2 to 91.2) for double bifid PM (both p=0.005), independent of septal thickness, use of b-blockers and/or calcium blockers and
resting heart rate.
Conclusions: Patients with HCM with abnormal PM have a higher degree of resting LVOT gradient, which is independent of septal thickness.
Patients with HCM with altered PM morphology—that is, anteroapical displacement of anterolateral PM or double bifid PMs, have a significantly higher prevalence of SAM or an elevated resting LVOT gradient, compared with those without.
The association between altered PMs and resting LVOT gradient appears to be independent of septal thickness, resting heart rate or use of drugs (b-blockers or calcium blockers, or both). A significant proportion of patients with HCM with abnormal PM morphology continued to have provocable LVOT gradient despite septal myectomy. Further prospective long-itudinal studies are required to determine if abnormal PM morphology is progressive and associated with adverse outcomes.
Also, it needs to be determined if surgical correction of abnormal PM morphology provides incremental value to septal myectomy/mitral valve repair alone.

+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
Prevalence of exercise-induced left ventricular outflow tract obstruction in symptomatic patients with non-obstructive hypertrophic cardiomyopathy

J S Shah, M T T Esteban, R Thaman, R Sharma, B Mist, A Pantazis, D Ward, S K Kohli, S P Page, C Demetrescu, E Sevdalis, A Keren, D Pellerin, W J McKenna and P M Elliott

Heart 2008;94;1288-1294; originally published online 21 Nov 2007;
doi:10.1136/hrt.2007.126003

ABSTRACT
Background: Resting left ventricular outflow tract obstruction (LVOTO) occurs in 25% of patients with hypertrophic cardiomyopathy (HCM) and is an important cause of symptoms and disease progression. The prevalence and clinical significance of exercise induced LVOTO in patients with symptomatic non-obstructive HCM is uncertain.
Methods and results: 87 symptomatic patients (43.3 (13.7) years, 67.8% males) with HCM and no previously documented LVOTO (defined as a gradient >30 mm Hg) underwent echocardiography during upright cardiopulmonary exercise testing: 54 patients (62.1%; 95% CI 51.5
to 71.6) developed LVOTO during exercise (latent LVOTO); 33 (37.9%; 95% CI 28.4 to 48.5) had neither resting nor exercise LVOTO (non-obstructive).
Patients with latent LVOTO were more likely to have systolic anterior motion of the mitral valve (SAM) at rest (relative risk 2.1, 95% CI
1.2 to 3.8; p=0.01), and higher peak oxygen consumption (mean difference: 10.3%, 95% CI 2.1 to 18.5; p=0.02) than patients with non-obstructive HCM.
The only independent predictors of D gradient during exercise were a history of presyncope/syncope, incomplete/complete SAM at rest and Wigle score (all p,0.05). Subsequent invasive reduction of LVOTO in 10
patients with latent obstruction and drug refractory symptoms resulted in improved functional class and less syncope/presyncope (all p,0.05).
Conclusions: Approximately two-thirds of patients with symptomatic non-obstructive HCM have latent LVOTO.
This study suggests that all patients with symptomatic non-obstructive HCM should have exercise stress echocardiography.
Over 60% of symptomatic patients with apparently nonobstructive hypertrophic cardiomyopathy have obstruction during exercise.
A history of presyncope/syncope and the presence of SAM are associated with the greatest changes in exercise-induced gradients.
The identification of latent obstruction as a cause of exertional symptoms should prompt more
vigorous pharmacological therapy, using combinations of drugs (including disopyramide) that would not be routinely employed in patients with non-obstructive HCM.
The use of invasive gradient reduction strategies (alcohol septal ablation and surgical myectomy) in patients with large exercise-induced gradients refractory to medical therapy can substantially
improve symptom status, but require further study in prospectively evaluated cohorts. The paradoxical relation between peak oxygen consumption and exercise-induced obstruction is intriguing and warrants further investigation.

Termination-of-resuscitation rules validated in cardiac arrest

Termination-of-resuscitation rules validated in cardiac arrest

24 September 2008

MedWire News: US researchers have validated two rules for identifying patients with out-of-hospital cardiac arrest (OHCA) who have little or no chance of survival.

The termination-of-resuscitation rules, developed by the Ontario Prehospital Life Support group, cover responders providing basic life support (BLS) and those providing advanced life support (ALS) to patients with OHCA.

The BLS rule has three criteria: event not witnessed by emergency medical services personnel; no automated external defibrillator used or manual shock applied in out-of-hospital setting; and no return of spontaneous circulation in out-of-hospital setting.

The ALS rule includes the BLS rule plus two additional criteria: arrest not witnessed by bystander; and no bystander-administered cardiopulmonary resuscitation.

The aim of the present study, by Comilla Sasson (University of Michigan, Ann Arbor) and team, was to validate the two rules using surveillance data prospectively submitted by emergency medical systems and hospitals in eight US cities between 2005 and 2008.

Sasson retrospectively applied the rules to 5505 adults with OHCA, 392 (7.1%) of whom survived to hospital discharge.

Of 2592 patients who met the BLS criteria, just five (0.2%) survived to discharge. The BLS rule therefore had a specificity of 0.987 and a positive predictive value of 0.998 for predicting mortality.

Of 1192 patients who met the ALS criteria, none survived to discharge. Accordingly, the ALS rule had a specificity of 1.000 and positive predictive value of 1.000.

"Had either rule been used to guide decisions to cease resuscitative efforts in the out-of-hospital setting, emergency medical systems could have substantially reduced the rate of emergency transports without appreciably worsening the rate of cardiac arrest survival," Sasson et al conclude.

"A prospective study is warranted to assess how well emergency medical systems implement either the BLS or ALS rule in clinical practice."

The study is reported in the Journal of the American Medical Association.

JAMA 2008; 300: 1432-1438