Elena Cervi

Phrenic stimulation: a challenge for cardiac resynchronization therapy.

Background—Phrenic stimulation (PS) may hinder left ventricular (LV) pacing. We prospectively observed its prevalence in consecutive patients with cardiac resynchronization therapy (CRT) devices. Methods and Results—In the years 2003 to 2006, 197 patients received a CRT device. PS and LV threshold measurements were carried out at implantation and at 6-month follow-up. LV reverse remodeling was assessed by echocardiography before implantation and at follow-up. LV lead placement was lateral/posterolateral in 86% of patients. Both PS and LV reverse remodeling occurred most frequently at the lateral/posterolateral LV pacing sites (P<0.001). PS was detected in 73 (37%) of patients and was clinically relevant in 41 (22%). The detection of PS at implantation had a poor sensitivity, as it occurred only in left lateral or sitting position in 27 patients. Ten patients (5%) underwent repeated surgery and 4 (2%) had their CRT turned off because of PS. At follow-up, we could manage PS noninvasively in 32 patients with a small PS-LV threshold difference: in 20 by cathode programmability (3 also thanks to automatic management of LV output) and in 12 (without cathode programmability) by programming the LV output as threshold +1 V. Conclusions—PS may seriously hinder CRT. A bipolar LV lead and cathode programmability are mandatory to avoid PS by changing the LV pacing vector at target sites for CRT. LV stability at target sites despite PS should also be pursued by these means. The automatic adjustment of LV pacing output is complementary in patients with a small PS-LV threshold difference.Background— Phrenic stimulation (PS) may hinder left ventricular (LV) pacing. We prospectively observed its prevalence in consecutive patients with cardiac resynchronization therapy (CRT) devices. Methods and Results— In the years 2003 to 2006, 197 patients received a CRT device. PS and LV threshold measurements were carried out at implantation and at 6-month follow-up. LV reverse remodeling was assessed by echocardiography before implantation and at follow-up. LV lead placement was lateral/posterolateral in 86% of patients. Both PS and LV reverse remodeling occurred most frequently at the lateral/posterolateral LV pacing sites ( P <0.001). PS was detected in 73 (37%) of patients and was clinically relevant in 41 (22%). The detection of PS at implantation had a poor sensitivity, as it occurred only in left lateral or sitting position in 27 patients. Ten patients (5%) underwent repeated surgery and 4 (2%) had their CRT turned off because of PS. At follow-up, we could manage PS noninvasively in 32 patients with a small PS-LV threshold difference: in 20 by cathode programmability (3 also thanks to automatic management of LV output) and in 12 (without cathode programmability) by programming the LV output as threshold +1 V. Conclusions— PS may seriously hinder CRT. A bipolar LV lead and cathode programmability are mandatory to avoid PS by changing the LV pacing vector at target sites for CRT. LV stability at target sites despite PS should also be pursued by these means. The automatic adjustment of LV pacing output is complementary in patients with a small PS-LV threshold difference. Received December 14, 2008; accepted June 10, 2009. # CLINICAL PERSPECTIVE {#article-title-2}

Exercise stress echocardiography is superior to rest echocardiography in predicting left ventricular reverse remodelling and functional improvement after cardiac resynchronization therapy

AIMS Cardiac resynchronization therapy (CRT) improves functional capacity and survival in heart failure. However, one-third of patients fail to respond to CRT. Resting left ventricular (LV) dyssynchrony assessed by echocardiography (ECHO) showed discordant results in identifying CRT responders. LV dyssynchrony can totally change during exercise. Aim of this study was to evaluate whether exercise dyssynchrony could select responders to CRT. METHODS AND RESULTS Sixty-four patients scheduled for CRT implantation performed bicycle exercise ECHO in semi-supine position on an exercise tilting table before and 6 months after CRT implantation. Tissue Doppler imaging (TDI) was acquired both at rest and during exercise to detect LV mechanical dyssynchrony. Predictive values for CRT response were 70% for rest TDI and 89% for exercise TDI (P = 0.01). Exercise LV dyssynchrony was the only parameter independently associated with follow-up improvement of rest ejection fraction and LV volume during multivariable analysis (P < 0.001). Functional improvement at 6-min walking test was statistically higher in patients with exercise dyssynchrony (P = 0.005), and not different considering rest dyssynchrony (P = 0.30). CONCLUSION Exercise intraventricular dyssynchrony assessed by exercise TDI ECHO is a strong independent predictor of CRT response. It could be used to select candidates for CRT, thus reducing ineffective implantations of biventricular pacemakers.

Interventricular Delay Interval Optimization in Cardiac Resynchronization Therapy Guided by Echocardiography Versus Guided by Electrocardiographic QRS Interval Width

Present devices for cardiac resynchronization therapy offer the possibility of tailoring the hemodynamic effect of biventricular pacing by optimization of the interventricular delay (VV) beyond atrioventricular (AV)-interval optimization. It was not yet defined whether a QRS width-based strategy may be a helpful tool for echocardiography for device programming. The aim of the study was to investigate the relation between VV-interval optimization guided by echocardiography and guided by QRS interval width. One hundred six patients with a cardiac resynchronization therapy device for > or =3 months were enrolled. All patients underwent echocardiographic AV and VV delay optimization. The AV interval was optimized according to the E wave-A wave (EA) interval and left ventricular filling time. At the optimal AV delay, VV optimization was performed by measuring the aortic velocity time integral at 5 different settings: simultaneous right and left ventricle output, left ventricle pre-excitation (left ventricle + 40 and 80 ms, respectively), and right ventricle pre-excitation (right ventricle + 40 and 80 ms, respectively). A 12-lead electrocardiogram was recorded and QRS duration was measured in the lead with the greatest QRS width. The electrocardiographic (ECG)-optimized VV interval was defined according to the narrowest achievable QRS interval among 5 VV intervals. The echocardiographic-optimized VV interval was left ventricle + 40 ms in 28 patients, left ventricle + 80 ms in 15 patients, simultaneous in 46 patients, right ventricle + 40 ms in 14 patients, and right ventricle + 80 ms in 3 patients. Significant concordance (kappa = 0.69, p <0.001) was found between the echocardiographic- and ECG-optimized VV interval. In conclusion, significant concordance appeared to exist during biventricular pacing between VV programming based on the shortest QRS interval at 12-lead ECG pacing and echocardiographic-guided VV-interval optimization. A combined ECG- and echocardiographic approach could be a less time-consuming solution in performing this operation.

Transcatheter aortic valve implantation with a self-expanding nitinol bioprosthesis: prediction of the need for permanent pacemaker using simple baseline and procedural characteristics.

Objective: To ascertain incidence and predictors of new permanent pacemaker (PPM) following transcatheter aortic valve implantation (TAVI) with the self‐expanding aortic bioprosthesis. Background: TAVI with the Medtronic Corevalve (MCV) Revalving System (Medtronic, Minneapolis, MN) has been associated with important post‐procedural conduction abnormalities and frequent need for PPM. Methods: Overall, 73 consecutive patients with severe symptomatic AS underwent TAVI with the MCV at two institutions; 10 patients with previous pacemaker and 3 patients with previous aortic valve replacement were excluded for this analysis. Clinical, echocardiographic, and procedural data were collected prospectively in a dedicated database. A standard 12‐lead ECG was recorded in all patients at baseline, after the procedure and predischarge. Decision to implant PPM was taken according to current guidelines. Logistic multivariable modeling was applied to identify independent predictors of PPM at discharge. Results: Patients exhibited high‐risk features as evidenced by advanced age (mean = 82.1 ± 6.2 years) and high surgical scores (logistic EuroSCORE 23.0 ± 12.8%, STS score 9.4 ± 6.9%). The incidence of new PPM was 28.3%. Interventricular septum thickness and logistic Euroscore were the baseline independent predictors of PPM. When procedural variables were included, the independent predictors of PPM were interventricular septum thickness (OR 0.52; 95% CI 0.32–0.85) and the distance between noncoronary cusp and the distal edge of the prosthesis (OR 1.37; 95% CI 1.03–1.83). Conclusions: Conduction abnormalities are frequently observed after TAVI with self‐expandable bioprosthesis and definitive pacing is required in about a third of the patients, with a clear association with depth of implant and small interventricular septum thickness.

Clinical Management of Atrial Fibrillation: Need for a Comprehensive Patient-Centered Approach

www.chestpubs.org Financial/nonfi nancial disclosures: The authors have reported to CHEST the following confl icts of interest: Dr Ziv is a consultant to Simbionix USA Inc, a medical simulation company. Within the past 3 years Dr Ziv was also consultant to CAE Healthcare, a medical simulation company. Drs Dunn and Murphy have reported that no potential confl icts of interest exist with any companies/organizations whose products or services may be discussed in this article . Correspondence to: William F. Dunn, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905; e-mail : dunn.william@mayo.edu

Peri-operative management of patients taking antithrombotic therapy: need for an integrated proactive approach

References 1 Sontag S. Illness as Metaphor, New York Review of Books, 1978. 2 Kon Z, Lackan N. Ethnic disparities in access to care in post apartheid South Africa. Am J Public Health 2008; 98: 2272–7 http://ajph.aphapublications.org/cgi/ content/abstract/98/12/2272 (Accessed 21 December 2010). 3 Stock R, Anyinam C. National government and health service policy in Africa. In: Collins R, ed. Problems in the History of Modern Africa. Markus Wiener Publishers, Princeton, NJ, 2008: 217–37. 4 Archives of the World Bank. Available online at: http://web.worldbank.org/WBSITE/EXTERNAL/EXT ABOUTUS/EXTARCHIVES/0,,content MDK:201215 26 pagePK:36726 piPK:36092 theSitePK:29506,00. html. 5 Sontag S. Aids and its Metaphors. New York: Farrar, Straus and Giroux, 1988. 6 Epstein, H. God and the Fight Against AIDS, New York Review of Books, New York, 2005. 7 Stockdill BC. Activism Against AIDS. Boulder, Colorado: Lynne Rienner Publishers, 2003. 8 Gruskin S, Mills E, Tarantola D. Health and human rights 1: history, principles and the practice of human rights. Lancet 2007; 370: 449–555. 9 The World Health Organization. Constitution of the World Health Organization. Geneva, 2010 http:// www.who.int/governance/eb/who_constitution_en. pdf. 10 The World Health Organization. Human RightsBased Approach to Health. Geneva, 2010 http://www. who.int/trade/glossary/story054/en/index.html. 11 Merson MH, O’Malley J, Serwadda D, Apisuk C, The history and challenge of HIV. Lancet 2008; 372: 475–88. 12 http://www.who.int/hpr/NPH/docs/declaration_almaata.pdf. 13 Brown T, Cueto M, Fee E. The World Health Organization and the transition from ‘International’ to ‘Global’ health. Am J Public Health 2006; 96: 62– 72. 14 Global Eonomic Governance Program, Oxford University, UK. www.globaleconomicgovernance.org. 15 Economic Governance for Health, London, UK. http://www.eg4health.org/. 16 Woods N. The challenge of good governance for the IMF and World Bank. World Dev 2000; 28: 823–41. 17 Simms C. Good governance at the World Bank. Lancet 2008; 371: 202–3. 18 Edwards B. Racial Discrimination at the World Bank. Foreign Policy in Focus, 19 June 2009. http:// www.fpif.org/articles/racial_discrimination_at_the_ world_bank. 19 Simms C. Donor, lender and research agencies response to the HIV crisis. In: Beck EJ, Mays N, Whiteside A, Zuniga JM, eds. The HIV Pandemic: Global and Local Implications, Oxford University Press, Oxford, UK, 2006: 608–21. 20 The World Bank. Investing in Health: Development Effectiveness in the Health, Nutrition, and Population Sectors. Washington, DC: World Bank, 1999. 21 World Bank Independent Evaluation Group. Committing to Results: Improving the Effectiveness of HIV ⁄ AIDS Assistance: An OED Evaluation of the World Bank’s Assistance for HIV ⁄ AIDS Control. Washington, DC: World Bank, 2005. 22 World Bank Independent Evaluation Group. 2006 Annual Review of Development Effectiveness: Getting Results [Report no 37161]. Washington, DC: World Bank, 2006. 23 World Bank Operations Evaluation Department. Committing to Results: Improving the Effectiveness of HIV ⁄ AIDS Assistance: An OED Evaluation of the World Bank’s Assistance for HIV ⁄ AIDS Control. Washington, DC: World Bank, 2005. 24 World Bank. Confronting AIDS: Public Priorities in a Global Epidemic. Oxford, UK: Oxford University Press for the World Bank, 1997: 245. 25 Brundtland GH. Director-General, World Health Organization XXIV World AIDS Conference, Barcelona, 9 July 2002. 26 United Nations, Resolution adopted by the General Assembly 55 ⁄ 2. United Nations Millennium Declaration, New York, 6 September 2000. http://www.un. org/millennium/declaration/ares552e.htm. 27 Szlezak N, Bloom B, Jamison D et al. The global health system: actors, norms and expectations in transition. PloS Medicine 2010; 7. http://www.plosmedi cine.org/article/info%3Adoi%2F10.1371%2Fjournal. pmed.1000183. 28 Global Health Watch II. An Alternative World Health Report. London and New York: Zed Books, 2008. 29 Fitchett J. The right to health in practice. Int J Clin Pract 2011; 65: 245–8. 30 Backman G, Hunt P, Khosla R et al. Health systems and the right to health: an assessment of 194 countries. Lancet 2008; 372: 2047–85.

Le tachicardie sopraventricolari in età pediatrica

Supraventricular tachycardias in children still remain a challenge not only for the pediatrician, but also for the adult cardiologist who is facing an infant in an emergency situation. This review examines the unique aspects of pediatric arrhythmias, with particular emphasis on acute treatment and pharmacological prophylaxis. All current treatment options are focused, from the “old drugs” to the “novel ablative techniques”: the first are often able to defer the second to a more suitable age, with fewer adverse effects and higher success rates. A brief account on Wolff-Parkinson-White issues concludes the review.

Follow-up of neonates with foetal and neonatal arrhythmias

Foetal arrhythmias occur in 1% of all pregnancies and the majority are benign, mainly ectopic beats. However, in about 10% of cases, sustained supraventricular tachycardia (SVT) or atrio-ventricular block (AVB) may cause heart failure, hydrops and eventually foetal death. An accurate analysis of the type of arrhythmia in utero is obtained by means of M-Mode and Doppler echocardiography. Foetal tachycardia is diagnosed when ventricular heart rate (HR) is faster than 180 bpm (up to 200–300 bpm). Paroxysmal SVT and atrial flutter (AF) are the most frequent causes of tachycardia, whereas ventricular tachycardia is very rare in the foetus. The perinatal management of SVT and AF consists of transplacental administration of antiarrhythmic drugs, usually digoxin as first choice and sotalol, flecainide and amiodarone as a second option or in combination. It is worth mentioning that in hydropic foetuses, transplacental distribution of digoxin may be impaired. Postnatal pharmacological treatment is usually successful but very premature babies with unstable haemodynamic conditions and with SVT are at risk, and treatment in utero could be preferable, even in presence of hydrops. Foetal bradyarrhythmia is diagnosed when HR is less than 100 bpm. The most frequent cause is AVB, and in about half of cases there is an associated congenital cardiac malformation; in the other half of cases, cardiac structure is normal and anti-Ro/SSA maternal antibodies are frequently present (in 80% of our series). In rare cases, foetal bradycardia is related to long QT (LQT) syndrome, either with 2:1 AVB or sinus bradycardia; in some cases, blocked premature beats may occur. Foetal bradycardia with congenital heart disease and/or hydrops has a poor prognosis. Efficacy of prenatal treatment for foetal AVB is somewhat discouraging and controversial, as beta stimulators and steroids have been reported to be effective in a minority of cases. Early delivery and neonatal pacing are necessary when foetal HR is less than 55–50 bpm and hydrops is developing. Early implant of a cardiac pace-maker (PMK) is not mandatory in neonates with normal cardiac structure, complete AVB and monitored HR above 50 bpm over the bulk of the day: it can be postponed depending on clinical condition. In our series of 14 prenatal AVB patients, three patients required neonatal PMK implantation. Data on postnatal follow-up of patients with foetal SVT are few: reports show that about 60–70% of patients develop postnatal arrhythmias, particularly those who did not convert to sinus rhythm prenatally. Foetal AF may also relapse in the first 24–48 h after birth. Although transesophageal overdrive pacing and cardioversion are more effective in AF patients, generally antiarrhythmic pharmacological treatment is successful in SVT. Medical treatment should be continued for the first year of life but the range is variable, as some patients may require longer treatment and eventually transcatheter ablation. Declaration of Interest: The authors report no conflicts of interest.

Phrenic StimulationCLINICAL PERSPECTIVE

Background—Phrenic stimulation (PS) may hinder left ventricular (LV) pacing. We prospectively observed its prevalence in consecutive patients with cardiac resynchronization therapy (CRT) devices. Methods and Results—In the years 2003 to 2006, 197 patients received a CRT device. PS and LV threshold measurements were carried out at implantation and at 6-month follow-up. LV reverse remodeling was assessed by echocardiography before implantation and at follow-up. LV lead placement was lateral/posterolateral in 86% of patients. Both PS and LV reverse remodeling occurred most frequently at the lateral/posterolateral LV pacing sites (P<0.001). PS was detected in 73 (37%) of patients and was clinically relevant in 41 (22%). The detection of PS at implantation had a poor sensitivity, as it occurred only in left lateral or sitting position in 27 patients. Ten patients (5%) underwent repeated surgery and 4 (2%) had their CRT turned off because of PS. At follow-up, we could manage PS noninvasively in 32 patients with a small PS-LV threshold difference: in 20 by cathode programmability (3 also thanks to automatic management of LV output) and in 12 (without cathode programmability) by programming the LV output as threshold +1 V. Conclusions—PS may seriously hinder CRT. A bipolar LV lead and cathode programmability are mandatory to avoid PS by changing the LV pacing vector at target sites for CRT. LV stability at target sites despite PS should also be pursued by these means. The automatic adjustment of LV pacing output is complementary in patients with a small PS-LV threshold difference.Background— Phrenic stimulation (PS) may hinder left ventricular (LV) pacing. We prospectively observed its prevalence in consecutive patients with cardiac resynchronization therapy (CRT) devices. Methods and Results— In the years 2003 to 2006, 197 patients received a CRT device. PS and LV threshold measurements were carried out at implantation and at 6-month follow-up. LV reverse remodeling was assessed by echocardiography before implantation and at follow-up. LV lead placement was lateral/posterolateral in 86% of patients. Both PS and LV reverse remodeling occurred most frequently at the lateral/posterolateral LV pacing sites ( P <0.001). PS was detected in 73 (37%) of patients and was clinically relevant in 41 (22%). The detection of PS at implantation had a poor sensitivity, as it occurred only in left lateral or sitting position in 27 patients. Ten patients (5%) underwent repeated surgery and 4 (2%) had their CRT turned off because of PS. At follow-up, we could manage PS noninvasively in 32 patients with a small PS-LV threshold difference: in 20 by cathode programmability (3 also thanks to automatic management of LV output) and in 12 (without cathode programmability) by programming the LV output as threshold +1 V. Conclusions— PS may seriously hinder CRT. A bipolar LV lead and cathode programmability are mandatory to avoid PS by changing the LV pacing vector at target sites for CRT. LV stability at target sites despite PS should also be pursued by these means. The automatic adjustment of LV pacing output is complementary in patients with a small PS-LV threshold difference. Received December 14, 2008; accepted June 10, 2009. # CLINICAL PERSPECTIVE {#article-title-2}

Phrenic StimulationCLINICAL PERSPECTIVE: A Challenge for Cardiac Resynchronization Therapy

Background—Phrenic stimulation (PS) may hinder left ventricular (LV) pacing. We prospectively observed its prevalence in consecutive patients with cardiac resynchronization therapy (CRT) devices. Methods and Results—In the years 2003 to 2006, 197 patients received a CRT device. PS and LV threshold measurements were carried out at implantation and at 6-month follow-up. LV reverse remodeling was assessed by echocardiography before implantation and at follow-up. LV lead placement was lateral/posterolateral in 86% of patients. Both PS and LV reverse remodeling occurred most frequently at the lateral/posterolateral LV pacing sites (P<0.001). PS was detected in 73 (37%) of patients and was clinically relevant in 41 (22%). The detection of PS at implantation had a poor sensitivity, as it occurred only in left lateral or sitting position in 27 patients. Ten patients (5%) underwent repeated surgery and 4 (2%) had their CRT turned off because of PS. At follow-up, we could manage PS noninvasively in 32 patients with a small PS-LV threshold difference: in 20 by cathode programmability (3 also thanks to automatic management of LV output) and in 12 (without cathode programmability) by programming the LV output as threshold +1 V. Conclusions—PS may seriously hinder CRT. A bipolar LV lead and cathode programmability are mandatory to avoid PS by changing the LV pacing vector at target sites for CRT. LV stability at target sites despite PS should also be pursued by these means. The automatic adjustment of LV pacing output is complementary in patients with a small PS-LV threshold difference.Background— Phrenic stimulation (PS) may hinder left ventricular (LV) pacing. We prospectively observed its prevalence in consecutive patients with cardiac resynchronization therapy (CRT) devices. Methods and Results— In the years 2003 to 2006, 197 patients received a CRT device. PS and LV threshold measurements were carried out at implantation and at 6-month follow-up. LV reverse remodeling was assessed by echocardiography before implantation and at follow-up. LV lead placement was lateral/posterolateral in 86% of patients. Both PS and LV reverse remodeling occurred most frequently at the lateral/posterolateral LV pacing sites ( P <0.001). PS was detected in 73 (37%) of patients and was clinically relevant in 41 (22%). The detection of PS at implantation had a poor sensitivity, as it occurred only in left lateral or sitting position in 27 patients. Ten patients (5%) underwent repeated surgery and 4 (2%) had their CRT turned off because of PS. At follow-up, we could manage PS noninvasively in 32 patients with a small PS-LV threshold difference: in 20 by cathode programmability (3 also thanks to automatic management of LV output) and in 12 (without cathode programmability) by programming the LV output as threshold +1 V. Conclusions— PS may seriously hinder CRT. A bipolar LV lead and cathode programmability are mandatory to avoid PS by changing the LV pacing vector at target sites for CRT. LV stability at target sites despite PS should also be pursued by these means. The automatic adjustment of LV pacing output is complementary in patients with a small PS-LV threshold difference. Received December 14, 2008; accepted June 10, 2009. # CLINICAL PERSPECTIVE {#article-title-2}