Removal of an active fixation coronary sinus pacing lead 5 years postimplant: A case report.

Active fixation for a lead in the coronary sinus may be essential to select the optimal left ventricular pacing site, maximize the effectiveness of cardiac resynchronization therapy (CRT) and avoid dislodgement. The Medtronic Attain Stability lead allows fixation through a side helix concentric with the lead body. Although electrical performance of such a lead is well known, evidence of extractability remains poor especially in the long term. We describe the removal of an Attain Stability lead 63 months after implantation which, to the best of our knowledge, is the longest implant duration that has ever been reported, in an 81-year-old male patient. It was successfully achieved using simple traction and rotation maneuvers, demonstrating the long-term removal feasibility of such device.

Remote assessment of QT interval: A new perspective for implantable cardiac monitors.

BACKGROUND: There is an unmet need for simple tools for monitoring QT intervals. The feasibility of measuring the QT interval on the single­lead subcutaneous electrocardiogram (subECG) recorded and transmitted by implantable cardiac monitors (ICMs) has never been tested. METHODS: We performed a standard ECG in patients who had already been implanted with a long sensing vector ICM (BIOMONITOR, Biotronik SE&Co.) to calculate the corrected QT interval in lead II (QTc ECG). The QTc was then evaluated on the subECG provided by ICM both by using the programmer printout (QTc subECG) and the snapshot transmitted via home monitoring (QTc HM). Values were compared with Bland-Altman analyses. RESULTS: The study cohort consisted of 23 ICM recipients (age 58 ± 19 years, 35% female) implanted mainly for unexplained syncope (78%). The mean QTc ECG interval was 404 ± 31 ms. The T-wave was visible and QTc could be calculated in all patients using the ICM programmer printout and in 21 (91%) patients remotely. The QTc subECG and QTc HM were 405 ± 34 and 406 ± 32 ms. Compared to the QTc ECG, Bland-Altman analyses revealed a bias of -0.9 (95% confidence interval: -6.8/4.9) ms and 0.1 (-12.7/12.9) ms for QTc subECG and QTc HM, respectively. CONCLUSIONS: The QTc interval can be reliably estimated on in-person and remote subECG in most patients without bias compared to the ECG lead II assessment. This technology has the potential to facilitate remote QT interval monitoring.

Reverse takotsubo cardiomyopathy followed by left ventricle outflow tract obstruction: A dangerous relay race.

Reverse takotsubo cardiomyopathy (rTTC) is a less frequent variant of takotsubo cardiomyopathy (TTC) with several differences about epidemiology and clinical aspects. While left ventricular outflow tract (LVOT) obstruction is relatively frequent in TTC patients, this complication has not been reported in the setting of rTTC yet. We describe the case of a female patient with rTTC complicated by LVOT obstruction and systolic anterior motion of mitral valve: the onset of these findings coincided with the regression of wall motion abnormalities. This dangerous "relay race" seems to be not casual but related to the characteristics of rTTC and should be always expected and prevented. .

Changes in oral anticoagulation for elective cardioversion: results from a European cardioversion registry.

Aims: In patients with atrial fibrillation (AF) pharmacological or electrical cardioversion may be performed to restore sinus rhythm. The procedure is associated with an increased risk of thromboembolic events, which can be significantly reduced by adequate anticoagulation (OAC). Our aim was to create a partly prospective, partly retrospective cardioversion registry, particularly focusing on OAC strategies in different European countries, and on emerging choice of OAC over time. Methods: From September 2014 to October 2015, cardioversions due to AF performed in six European city hospitals in five European countries (Hungary: Budapest-1 and -2; Italy: Bari and Pisa; France: Amiens; Spain: Madrid; and Lithuania: Kaunas) were recorded in the registry. Results: A total of 1101 patients (retrospective/prospective: 679/422, male/female: 742/359, mean age: 67.3 years ± 11.2) were registered. Most of the cardioversions were electrical (97%). Oral anticoagulants were administered in 87% of the patient, the usage of non-VKA oral anticoagulants (NOACs) vs Vitamin K antagonists (VKA) was 31.5% vs 68.5%, respectively. Seventy seven percent of the patients were given oral anticoagulants more than 3 weeks prior to the procedure, and 86% more than 4 weeks after the procedure. When using VKA, international normalized ratio (INR) at cardioversion was above 2.0 in 76% of the cases. A decline in VKA usage (P = 0.033) in elective cardioversion over approximately 1 year was observed. During the observation period, there was an increase in apixaban (P < 0.001), a slight increase in rivaroxaban (P = 0.028) and no changes in dabigatran (P = 0.34) usage for elective cardioversion. There were differences in use of OAC between the countries: Spain used most VKA (89%), while France used least VKA (39%, P < 0.001). Conclusion: According to current AF guidelines, NOACs are adequate alternatives to VKA for thromboembolic prevention in AF patients undergoing elective cardioversion. Our results indicate that NOAC use is increasing and there is a significant decrease in VKA use.

Septal rupture with right ventricular wall dissecting haematoma communicating with left ventricle after inferior myocardial infarction.

We report the case of an 86-year-old man referred for abdominal pain and ECG signs of inferior myocardial infarction. Transthoracic, transoesophageal and contrast echocardiographs showed a septal intra-mural haematoma, dissecting the right ventricle wall and partially obliterating the right ventricle lumen. A patent communication with left ventricle with extensive wall thrombosis was present at Doppler examination within dissecting haematoma. Although the patient refused any surgical treatment, a 3-month follow-up was uneventful.

SCN5A polymorphism restores trafficking of a Brugada syndrome mutation on a separate gene.

BACKGROUND: Brugada syndrome is associated with a high risk of sudden cardiac death and is caused by mutations in the cardiac voltage-gated sodium channel gene. Previously, the R282H-SCN5A mutation in the sodium channel gene was identified in patients with Brugada syndrome. In a family carrying the R282H-SCN5A mutation, an asymptomatic individual had a common H558R-SCN5A polymorphism and the mutation on separate chromosomes. Therefore, we hypothesized that the polymorphism could rescue the mutation. METHODS AND RESULTS: In heterologous cells, expression of the mutation alone did not produce sodium current. However, coexpressing the mutation with the polymorphism produced significantly greater current than coexpressing the mutant with the wild-type gene, demonstrating that the polymorphism rescues the mutation. Using immunocytochemistry, we demonstrated that the R282H-SCN5A construct can traffic to the cell membrane only in the presence of the H558R-SCN5A polymorphism. Using fluorescence resonance energy transfer and protein fragments centered on H558R-SCN5A, we demonstrated that cardiac sodium channels preferentially interact when the polymorphism is expressed on one protein but not the other. CONCLUSIONS: This study suggests a mechanism whereby the Brugada syndrome has incomplete penetrance. More importantly, this study suggests that genetic polymorphisms may be a potential target for future therapies aimed at rescuing specific dysfunctional protein channels.

Early and late determinants of C-reactive protein release in patients with acute coronary syndrome.

Increased levels of C-reactive protein (CRP) could be detected in subjects with acute coronary syndrome (ACS). Several factors, atherosclerosis, coronary flow impairment, myocardial necrosis, each one acting during a different, earlier or later, phase of ACS, are supposed to be involved in CRP release in case of ACS. Role and relevance of each factor, not mutually exclusive, still need to be comparatively evaluated but a cooperative synergism could be presumably hypothesized.

C-reactive protein in patients with acute coronary syndrome: correlation with diagnosis, myocardial damage, ejection fraction and angiographic findings.

BACKGROUND: C-reactive protein (CRP) plasmatic levels increase in patients with acute coronary syndromes (ACS). Correlations between CRP levels, myocardial functional damage and cardiomyocyte lysis remain to be defined. METHODS: 192 consecutive patients with acute coronary syndromes (64.97 +/- 11.08 mean age, 71.35% male gender) were included in the study; 138 patients (71.87%) were discharged with an acute myocardial infarction (AMI) diagnosis (28 with non Q-wave AMI) and 54 with an unstable angina (UA) diagnosis (28.13%). In all patients CRP, CK, LDH, CK-MB and troponin I plasmatic concentrations were evaluated every 6 h for 48 h and every 24 h for the following 2 days from the onset of symptoms. Ejection fraction was estimated by bidimensional echocardiography and extension of myocardial lysis by cardiac enzymes plasmatic release. 92 patients (67 with AMI, 25 with UA) underwent coronary-angiography. Incidence of adverse cardiac events was recorded in a 6 months follow up. RESULTS: Mean CRP levels in Q-wave MI showed a statistically significant increase in the different blood samples with baseline. Mean CRP levels of the three groups were not statistically different at baseline and after 6, 12, and 18 h. Q-wave AMI CRP levels showed a statistically significant difference as against non Q-wave AMI at 36 (p < 0.05), 48 (p < 0.05) and 72 h (p < 0.05) and UA at 24 (p < 0.01), 30 (p < 0.01), 48 (p < 0.0001), 72 (p = 0.0001) and 96 h (p = 0.0003); non Q-wave AMI CPR levels showed a statistically significant difference as against UA at 48 h (p < 0.01). CRP peak mean levels were significantly different when comparing Q-wave AMI patients with UA patients (8.21 +/- 7.85 vs. 2.75 +/- 3.33 mg/dl, p < 0.001). In patients with Q-wave AMI there was a correlation between CRP peak concentrations and CK (r = 0.264, p = 0.008) and LDH (r = 0.32, p = 0.001), while correlation with CK-MB peak concentrations was not statistically significant (r = 0.196, p = 0.051). In the same patient group, there was also a correlation between CRP plasmatic concentrations and troponin I plasmatic concentrations from the 30th to 96th h after the onset of symptoms (r = 0.38-0.53, p < 0.05). No correlation was found between CRP levels and ejection fraction and angio-coronarography findings (number of stenotic vessels, culprit lesions, ruptured plaques). Peak CRP levels were associated in a 6 months follow up with an increased incidence of major adverse cardiac events (MACEs) in patients with Q-wave AMI (HR 1.1649, 95% C.I. 1.0197-1.3307, p < 0.05). CONCLUSIONS: CRP plasmatic concentrations showed a different release curve in patients with Q-wave AMI in comparison with patients with non Q-wave AMI and with patients with UA. CRP peak concentrations did not correlate with ejection fraction and angiographic findings, but correlate with incidence of MACE. The increase in CRP levels during Q-wave MI seems to be linked to the extension of myocardial damage rather than pre-existing inflammation.

Non-antiarrhythmic drugs for the prevention of cardiac arrhythmias.

It is noteworthy that drugs having a significant impact in preventing arrhythmias (atrial or ventricular) are those with no direct specific antiarrhythmic electrophysiologic properties. Specifically, drugs able to interfere with the renin-angiotensin system and the n-3 fatty acids seem to play a relevant role as antiarrhythmics, even if they do not act in the typical manner. Angiotensin-converting enzyme (ACE) inhibitors decrease the incidence of arrhythmias in patients with decreased left ventricular function. The main reduction is linked to a decrease of ventricular arrhythmias, while several studies have suggested that ACE-inhibitors may also decrease the burden of atrial fibrillation. Furthermore, many of angiotensin receptor blockers and spironolactone have been shown to have antiarrhythmic properties. n-3 polyunsaturated fatty acids (PUFAs) are known to be antiarrhythmic as well. Their effects on the fast voltage-dependent sodium current I(NA), inhibition of I(Ca2+) and the K+ channel modulation explain their antiarrhythmic properties. For these reasons the renin-angiotensin system blockade and the n-3 PUFA intake may provide simple and safe protection from cardiac arrhythmias.

QT-interval prolongation in right precordial leads: an additional electrocardiographic hallmark of Brugada syndrome.

OBJECTIVES: The aim of this study was to evaluate whether the occurrence of the Brugada Syndrome typical electrocardiogram (ECG) pattern (i.e., right bundle branch block, coved-type ST-segment elevation, and T-wave inversion in the right precordial leads) is characterized by a concomitant lengthening of QT intervals in the right precordial leads. BACKGROUND: It has been suggested that the typical ECG pattern of Brugada syndrome is due to a decreased net inward current during phase 1 of the action potential, which also leads to its prolongation in the right epicardium. METHODS: Thirty-two subjects (19 males) age 37 +/- 15 years with a suspicious baseline ECG, or who were relatives of Brugada syndrome patients, underwent 12-lead ECG before and after the administration of flecainide. RESULTS: The flecainide test was negative in 14 and positive in 18 subjects. After flecainide administration, the positive ECGs were characterized by a greater QT interval corrected for heart rate (QTc) prolongation in the right precordial leads than that in the negative ECGs (78.2 +/- 35.5 ms vs. 22.0 +/- 28.4 ms in V(1) and 107.1 +/- 43.8 ms vs. 26.7 +/- 30.1 ms in V(2); p < 0.01), whereas there was no difference in the QTc prolongation in the left precordial leads (55.2 +/- 25.3 ms vs. 35.1 +/- 28.1 ms in V(5) and 53.1 +/- 32.8 ms vs. 27.3 +/- 22.4 ms in V(6); p = NS). CONCLUSIONS: In accordance with the electrophysiological background, the typical ECG pattern of Brugada syndrome is also characterized by a considerable prolongation of the QT interval in right precordial leads.