PVC induced cardiomyopathy: Difference between revisions
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Treatment for PVC-induced cardiomyopathy focuses on suppressing PVCs and reducing PVC burden, that could subsequently result in ventricular function improvement. Treatment methods include pharmacological therapy with anti-arrhythmic drugs and catheter ablation. | Treatment for PVC-induced cardiomyopathy focuses on suppressing PVCs and reducing PVC burden, that could subsequently result in ventricular function improvement. Treatment methods include pharmacological therapy with anti-arrhythmic drugs and catheter ablation. | ||
* '''Medical therapy:''' | * '''Medical therapy:''' | ||
Pharmacotherapy is the first treatment | Pharmacotherapy is the first treatment option for asymptomatic or mildly symptomatic patients without any [[structural heart disease]].<ref name="pmid12486439">{{cite journal| author=Krittayaphong R, Bhuripanyo K, Punlee K, Kangkagate C, Chaithiraphan S| title=Effect of atenolol on symptomatic ventricular arrhythmia without structural heart disease: a randomized placebo-controlled study. | journal=Am Heart J | year= 2002 | volume= 144 | issue= 6 | pages= e10 | pmid=12486439 | doi=10.1067/mhj.2002.125516 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12486439 }}</ref> There are several [[Antiarrhythmic agent|anti-arrhythmic drugs]] available such as [[Beta blockers|beta-blockers]], [[Calcium channel blocker|calcium channel blockers]], [[flecainide]], [[propafenone]], [[amiodarone]] or [[sotalol]] with varying effectiveness and side effects. [[Beta blockers|Beta-blockers]] are usually considered as a first line therapy, due to their low adverse effects and potential secondary benefits. In patients with no symptoms of [[Congestive heart failure|heart failure]], [[Calcium channel blocker|non-dihydropyridine calcium channel blockers]] are reasonable alternatives.<ref name="pmid237410582">{{cite journal| author=WRITING COMMITTEE MEMBERS. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE et al.| title=2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. | journal=Circulation | year= 2013 | volume= 128 | issue= 16 | pages= e240-327 | pmid=23741058 | doi=10.1161/CIR.0b013e31829e8776 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23741058 }}</ref> However, these two groups have only modest efficacy in reducing PVC burden. Moreover, whether they could significantly improve [[Ejection fraction|LVEF]] is still among debate. For instance, a study reported a 36% reduction of PVC burden with [[Beta blockers|beta-blockers]] and no effect on [[Ejection fraction|LVEF]].<ref name="pmid24157533" /> | ||
Antiarrhythmic drugs are stronger PVC suppressors. Studies have demonstrated reduced PVC counts by 83% in patients treated with class I antiarrhythmics compared with 70% reduction with | [[Antiarrhythmic agent|Antiarrhythmic drugs]] are stronger [[Premature ventricular contraction|PVC]] suppressors. Studies have demonstrated reduced PVC counts by 83% in patients treated with class I antiarrhythmics compared with 70% reduction with [[sotalol]]. [[Amiodarone]] had the highest efficacy with an 84% reduction of PVC counts. Except for [[amiodarone]], [[Antiarrhythmic agent|antiarrhythmic medicarions]] have no role in improving survival despite their higher efficacy. Due to their adverse effects such as negative [[Inotrope|inotropic]] and proarrhythmic effects, they are not recommended for treating frequent PVCs in [[Congestive heart failure|CHF]] patients.<ref name="pmid1900101">{{cite journal| author=Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH et al.| title=Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. | journal=N Engl J Med | year= 1991 | volume= 324 | issue= 12 | pages= 781-8 | pmid=1900101 | doi=10.1056/NEJM199103213241201 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1900101 }}</ref><ref name="pmid1377359">{{cite journal| author=Cardiac Arrhythmia Suppression Trial II Investigators| title=Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. | journal=N Engl J Med | year= 1992 | volume= 327 | issue= 4 | pages= 227-33 | pmid=1377359 | doi=10.1056/NEJM199207233270403 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1377359 }}</ref><ref name="pmid8691967">{{cite journal| author=Waldo AL, Camm AJ, deRuyter H, Friedman PL, MacNeil DJ, Pauls JF et al.| title=Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD Investigators. Survival With Oral d-Sotalol. | journal=Lancet | year= 1996 | volume= 348 | issue= 9019 | pages= 7-12 | pmid=8691967 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8691967 }}</ref><ref name="pmid18565860">{{cite journal| author=Køber L, Torp-Pedersen C, McMurray JJ, Gøtzsche O, Lévy S, Crijns H et al.| title=Increased mortality after dronedarone therapy for severe heart failure. | journal=N Engl J Med | year= 2008 | volume= 358 | issue= 25 | pages= 2678-87 | pmid=18565860 | doi=10.1056/NEJMoa0800456 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18565860 }}</ref> [[Amiodarone]], however, is the most effective drug to reduce PVC burden without increasing mortality rate in patients with advanced [[Congestive heart failure|CHF]]. It is also effective on [[Left ventricle|left ventricular]] function improvement.<ref name="pmid9581582" /> | ||
* '''Ablation:''' | * '''Ablation:''' | ||
==References == | ==References == | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 14:57, 18 April 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Farbod Zahedi Tajrishi, M.D.
Overview
PVC-induced cardiomyopathy has been a controversial subject since its introduction. The concept of the disease is mainly based on the overwhelming evidence suggesting that frequent PVCs may cause, or at least play a role in the development of cardiomyopathy. However, in addition to the absence of a clear definition for the condition, the mechanism for the development of this condition is not yet understood.
Historical perspective
In 1998, a study demonstrated that treating patients with frequent PVCs ( > 20,000 per day ) and ventricular dysfunction with amiodarone could significantly improve LVEF.[1] This result led to the initial assumption that frequent PVCs might cause a reversible form of cardiomyopathy and thus, the concept of PVC-induced cardiomyopathy as a separate entity was formed. Since then, multiple studies have attempted to clarify the nature and the features of the disease. However, the mechanisms through which frequent PVCs can cause ventricular dysfunction remain mainly unknown. Initial studies suggested that PVC-induced cardiomyopathy was essentially a tachycardia-induced cardiomyopathy as seen with other arrhythmias such as atrial fibrillation.[2] This hypothesis was rejected, however, because many patients with PVC-induced cardiomyopathy had normal average heart rates.[3]
Pathophysiology
The exact pathogenesis of PVC-induced cardiomyopathy is not fully understood.
Causes and risk factors
| Risk factors (predictors) | Reports of different studies |
|---|---|
| PVC burden | |
| PVC QRS duration | |
| PVC coupling interval | |
| Interpolated PVCs |
Natural history, complications, and prognosis
History and symptoms
Physical exam
Electrocardiogram
Echocardiography
Treatment
Treatment for PVC-induced cardiomyopathy focuses on suppressing PVCs and reducing PVC burden, that could subsequently result in ventricular function improvement. Treatment methods include pharmacological therapy with anti-arrhythmic drugs and catheter ablation.
- Medical therapy:
Pharmacotherapy is the first treatment option for asymptomatic or mildly symptomatic patients without any structural heart disease.[5] There are several anti-arrhythmic drugs available such as beta-blockers, calcium channel blockers, flecainide, propafenone, amiodarone or sotalol with varying effectiveness and side effects. Beta-blockers are usually considered as a first line therapy, due to their low adverse effects and potential secondary benefits. In patients with no symptoms of heart failure, non-dihydropyridine calcium channel blockers are reasonable alternatives.[6] However, these two groups have only modest efficacy in reducing PVC burden. Moreover, whether they could significantly improve LVEF is still among debate. For instance, a study reported a 36% reduction of PVC burden with beta-blockers and no effect on LVEF.[3]
Antiarrhythmic drugs are stronger PVC suppressors. Studies have demonstrated reduced PVC counts by 83% in patients treated with class I antiarrhythmics compared with 70% reduction with sotalol. Amiodarone had the highest efficacy with an 84% reduction of PVC counts. Except for amiodarone, antiarrhythmic medicarions have no role in improving survival despite their higher efficacy. Due to their adverse effects such as negative inotropic and proarrhythmic effects, they are not recommended for treating frequent PVCs in CHF patients.[7][8][9][10] Amiodarone, however, is the most effective drug to reduce PVC burden without increasing mortality rate in patients with advanced CHF. It is also effective on left ventricular function improvement.[1]
- Ablation:
References
- ↑ 1.0 1.1 Duffee DF, Shen WK, Smith HC (1998). "Suppression of frequent premature ventricular contractions and improvement of left ventricular function in patients with presumed idiopathic dilated cardiomyopathy". Mayo Clin Proc. 73 (5): 430–3. doi:10.1016/S0025-6196(11)63724-5. PMID 9581582.
- ↑ Ellis ER, Josephson ME (2013). "Heart failure and tachycardia-induced cardiomyopathy". Curr Heart Fail Rep. 10 (4): 296–306. doi:10.1007/s11897-013-0150-z. PMID 23963583.
- ↑ 3.0 3.1 Zhong L, Lee YH, Huang XM, Asirvatham SJ, Shen WK, Friedman PA; et al. (2014). "Relative efficacy of catheter ablation vs antiarrhythmic drugs in treating premature ventricular contractions: a single-center retrospective study". Heart Rhythm. 11 (2): 187–93. doi:10.1016/j.hrthm.2013.10.033. PMID 24157533.
- ↑ Lee AK, Deyell MW (2016). "Premature ventricular contraction-induced cardiomyopathy". Curr Opin Cardiol. 31 (1): 1–10. doi:10.1097/HCO.0000000000000236. PMID 26599061.
- ↑ Krittayaphong R, Bhuripanyo K, Punlee K, Kangkagate C, Chaithiraphan S (2002). "Effect of atenolol on symptomatic ventricular arrhythmia without structural heart disease: a randomized placebo-controlled study". Am Heart J. 144 (6): e10. doi:10.1067/mhj.2002.125516. PMID 12486439.
- ↑ WRITING COMMITTEE MEMBERS. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE; et al. (2013). "2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines". Circulation. 128 (16): e240–327. doi:10.1161/CIR.0b013e31829e8776. PMID 23741058.
- ↑ Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH; et al. (1991). "Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial". N Engl J Med. 324 (12): 781–8. doi:10.1056/NEJM199103213241201. PMID 1900101.
- ↑ Cardiac Arrhythmia Suppression Trial II Investigators (1992). "Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction". N Engl J Med. 327 (4): 227–33. doi:10.1056/NEJM199207233270403. PMID 1377359.
- ↑ Waldo AL, Camm AJ, deRuyter H, Friedman PL, MacNeil DJ, Pauls JF; et al. (1996). "Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD Investigators. Survival With Oral d-Sotalol". Lancet. 348 (9019): 7–12. PMID 8691967.
- ↑ Køber L, Torp-Pedersen C, McMurray JJ, Gøtzsche O, Lévy S, Crijns H; et al. (2008). "Increased mortality after dronedarone therapy for severe heart failure". N Engl J Med. 358 (25): 2678–87. doi:10.1056/NEJMoa0800456. PMID 18565860.