PVC induced cardiomyopathy: Difference between revisions
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== Treatment == | == 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 choice 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 anti-arrhythmic drugs available such as beta-blockers, calcium channel blockers, felcainide, propafenone, amidarone or satolol 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.<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 LVEF is still among debate. For instance, a study reported a 36% reduction of PVC burden with beta-blockers and no effect on 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 satolol. 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.<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> 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.<ref name="pmid9581582" /> | |||
* '''Ablation:''' | |||
==References == | ==References == | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 16:10, 7 April 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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
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 choice 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, felcainide, propafenone, amidarone or satolol 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 satolol. 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] 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.