Cardiovascular Journal of Africa: Vol 32 No 5 (SEPTEMBER/OCTOBER 2021)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 32, No 5, September/October 2021 252 AFRICA ventricular myocardium to maximise the systolic pump function. This is facilitated by normal conduction via the His–Purkinje system and coupled synchronous mechanical contraction. Electrical activation originating within the ventricular myocardium with PVCs, on the other hand, causes an inefficient mechanical ventricular contraction. Furthermore, when persisting on a repetitive long-term basis, this dyssynchronous ventricular contraction presumably leads to deterioration in LV systolic function through asymmetrically increasing the wall thickness in the late-activated regions, and altered myocardial blood flow. 20 On the other hand, more than 60% of the PVC patients had two or more co-morbidities, mainly diabetes mellitus, ischaemic heart disease and hypertension. PVCs are associated with a wide range of risk factors, including co-morbidities and increased body weight. Recently, von Rotz and colleagues performed a population-based study on 2 048 healthy adults in order to evaluate different risk factors for PVCs. They found that the presence of one or more co-morbidities was a significant risk factor for high PVCs. 21 Notably, catheter ablation of PVCs improves LV function. Akkaya and colleagues investigated the effects of catheter ablation of PVCs on parameters of LV function in 74 patients who underwent catheter ablation for symptomatic PVCs. They reported significant improvements in the LVEDD, LVESD and E/E ′ ratio after the ablation. 22 By contrast, Ling et al. comparedventricular function, assessed by 2D and real-time 3D speckle-tracking echocardiography, between patients with frequent PVCs and healthy controls. The results showed no significant differences between patients with PVCs and the healthy group in terms of LVEDD, LVESV and other 2D echocardiographic variables. 23 Study limitations This study has a number of limitations. The sample size of the included patients was relatively small and the study was a single-centre cohort, which may affect the generalisability of our findings. Moreover, we used conventional echocardiography for the assessment of systolic and diastolic function. The current literature shows that assessment of LVEF, LV size and trans-mitral blood flow by conventional echocardiography has limitations and hence is not satisfactory for accurate estimation of the real haemodynamic and fluid status. Another limitation is the absence of patient-centred long-term outcomes. Conclusion Patients with frequent PVCs exhibited significant LV systolic and diastolic dysfunction and also LV remodelling. The presence of frequent PVCs was found to be a significant independent predictor of impaired LVEF, especially in patients with co-morbidities. We found a strong association of PVC burden with LV filling pressure. Therefore, despite the prognosis in patients with frequent PVCs being considered relatively benign, attention should be paid to the progression of LV dysfunction during a long-term observation, especially in patients with a high PVC prevalence. Both the possible influence of premature beat load on cardiac function and the cut-off warrant further clinical studies. We also recommend further studies to confirm the association of PVC burden and LV filling pressure along with the effect of reducing filling pressure on managing PVCs. We acknowledge the Department of Cardiology, Suez Canal University for its support in performing this study. The study was partially funded by the Suez Canal University. References 1. Lee AKY, Deyell MW. Premature ventricular contraction-induced cardiomyopathy. Curr Opin Cardiol 2016; 31 : 1–10. 2. Gopinathannair R, Etheridge SP, Marchlinski FE, Spinale FG, Lakkireddy D, Olshansky B. Arrhythmia-induced cardiomyopathies mechanisms, recognition, and management . J Am Coll Cardiol 2015; 66 : 1714–1728. 3. Yarlagadda RK, Iwai S, Stein KM, Markowitz SM, Shah BK, Cheung JW, et al . Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract. Circulation 2005; 112 : 1092–1097. 4. Cha YM, Lee GK, Klarich KW, Grogan M. Premature ventricu- lar contraction-induced cardiomyopathy: A treatable condition. Circ Arrhythmia Electrophysiol 2012; 5 : 229–236. 5. Ribeiro WN, Yamada AT, Grupi CJ, da Silva GT, Mansur AJ. Premature atrial and ventricular complexes in outpatients referred from a primary care facility. PLoS One 2018; 13 (9): e0204246. 6. Karaman K, Karayakali M, Arisoy A, Akar I, Ozturk M, Yanik A, et al . Is there any relationship between myocardial repolarization param- eters and the frequency of ventricular premature contractions? Arq Bras Cardiol 2018; 110 (6): 534–541. 7. Wang Y, Eltit JM, Kaszala K, Tan A, Jiang M, Zhang M, et al . Cellular mechanism of premature ventricular contraction-induced cardiomyopa- thy. Heart Rhythm 2014; 11 (11): 2064–2072. 8. Park Y, Kim S, Shin J, Reum OH, Ji Shin E, Hoon Lee J, et al . Frequent premature ventricular complex is associated with left atrial enlargement in patients with normal left ventricular ejection fraction. Pacing Clin Electrophysiol 2014; 37 : 1455–1461. 9. Niwano S, Wakisaka Y, Niwano H, Fukaya H, Kurokawa S, Kiryu M, et al . Prognostic significance of frequent premature ventricular contrac- tions originating from the ventricular outflow tract in patients with normal left ventricular function. Heart 2009; 95 : 1230–1237. 10. Takahashi S, Mine T, Ashida K, Kishima H, Masuyama T, Ishihara M. Left ventricular inflow velocity pattern in patients with symptomatic premature ventricular contraction. Circ J 2020; 84 : 26–32. 11. Park J-H, Marwick TH. Use and limitations of E/e’ to assess left ventric- ular filling pressure by echocardiography. J Cardiovasc Ultrasound 2011; 19 : 169–173. 12. Zaborska B, Stec S, Flasi ń ska K, Pilu ś A, Kułakowski P. [Echo- cardiography and tissue Doppler imaging in assessment of haemody- namics in patients with idiopathic, premature ventricular complexes]. Pol Merkur Lekarski 2006; 20 : 302–304. 13. Duffee DF, Shen W-K, Smith HC. Suppression of frequent premature ventricular contractions and improvement of left ventricular function in patients with presumed idiopathic dilated cardiomyopathy. Mayo Clin Proc 1998; 7 3: 430–433. 14. Latchamsetty R, Bogun F. Premature ventricular complexes and prema- ture ventricular complex induced cardiomyopathy. Curr Probl Cardiol 2015; 40 : 379–422. 15. Kanei Y, Friedman M, Ogawa N, Hanon S, Lam P, Schweitzer P. Frequent premature ventricular complexes originating from the right ventricular outflow tract are associated with left ventricular dysfunction.

RkJQdWJsaXNoZXIy NDIzNzc=