Presence Of Premature Ventricular Complexes Research Articles

The association between exercise-induced ventricular premature contractions and long-term mortality in patients without coronary artery disease

Abstract Background/Introduction The treadmill exercise test is widely used clinical test to determine cardiovascular risk and mortality, regardless of clinical risk factors (1). ST-segment changes detected in the exercise test are shown to predict myocardial ischemia (2) and premature ventricular complexes (PVCs) are frequently observed during exercise stress testing (3). Exercise-related PVC is observed in 14% to 23% of healthy individuals without significant heart disease (4,5). The literature on the role of PVCs observed during treadmill exercise testing in predicting prognosis is controversial. Purpose Therefore, we aimed to evaluate the clinical results of PVCs seen during exercise testing in patients who had been diagnosed with non-obstructive coronary artery disease after coronary angiography. Methods The study population consisted of 1624 consecutive patients who were considered high risk according to the Duke treadmill risk score and had no significant stenosis on coronary angiogram from January 2016 to April 2021. Patients with previous history of coronary revascularization, previous myocardial infraction, heart failure, moderate or severe heart valve disease, congenital heart disease, cardiomyopathy, bundle branch block, and left ventricular hypertrophy were excluded from the study. The primary endpoints of the study were long-term all-cause mortality of patients who had PVCs during the exercise test or during the resting phase. Results The long-term mortality was observed in 53 patients out of 1624 patients in the mean follow-up of 47 months. PVCs was observed in 293 (18.7%) patients without long-term mortality, while PVCs was observed in 24 (45.3%) patients with long-term mortality (p<0.001). The model adjusted for all covariates showed that the presence of PVCs in the recovery phase (p<0.007, HR (95% CI) 2.244 (1.244 – 4.047)) and advanced age (p<0.001, HR (95% CI) 1.194 (1.143 – 1.247)) were associated with long-term all-cause mortality (Figure 1). Considering Kaplan-Meier curve, individuals with PVCs in recovery had significantly higher risk of long-term mortality compared with those with without PVCs (log-rank statistic: 22.47, p<0.001) (Figure 2). Conclusion(s) The study highlights that PVCs monitored in the recovery phase of the treadmill exercise test were associated with long -term mortality in patients without structural heart disease and coronary artery disease.Figure 2Figure 1

The Association between Exercise-Induced Ventricular Premature Contractions and Long-Term Mortality in Patients without Obstructive Coronary Artery Disease.

The treadmill exercise test is widely used to determine cardiovascular risk and mortality. Premature ventricular complexes (PVCs) are frequently observed during exercise stress testing. The literature on the role of PVCs observed during treadmill exercise testing in predicting prognosis is controversial. Hence, we aimed to evaluate the clinical results of PVCs seen during exercise testing in patients without obstructive coronary artery disease confirmed by coronary angiography (CAG). The study population consisted of 1624 consecutive patients who were considered high risk according to the Duke treadmill risk score and had no significant stenosis on CAG from January 2016 to April 2021. The primary endpoints of the study were long-term all-cause mortality of patients who had PVCs during the exercise test or during the resting phase. Long-term mortality was observed in 53 of the 1624 patients after a mean follow-up of 47 months. PVCs were observed in 293 (18.7%) patients without long-term mortality, and in 24 (45.3%) patients with long-term mortality (p < 0.001). The model adjusted for all covariates showed that the presence of PVCs in the recovery phase [p < 0.007, hazard ratio (HR) (95% confidence interval (CI)) 2.244 (1.244-4.047)] and advanced age [p < 0.001, HR (95% CI) 1.194 (1.143-1.247)] were associated with long-term all-cause mortality. PVCs observed during treadmill exercise testing and the recovery phase were related to long-term mortality in patients without obstructive coronary artery disease.

Impact on clinical outcome of ventricular arrhythmias in patients undergoing transcatheter aortic valve implantation (TAVI)

Abstract Background Transcatheter aortic valve implantation (TAVI) in the treatment of severe aortic stenosis has considerably grown in the latest years. There are limited data, however, about predictors of long-term prognosis in this population. Particularly, whether ventricular arrhythmic burden is associated with clinical outcome has poorly been investigated. Purpose The aim of our study was to investigate the association between ventricular arrhythmias and adverse clinical outcomes in patients undergoing TAVI. Methods We performed a 24-hour 3-channel ECG Holter monitoring (HM) in 267 consecutive patients who underwent TAVI for severe aortic stenosis at our Centre within 30 days from a successful procedure (average 10.2 days, range 2-30). For each patient we obtained the number of premature ventricular complexes (PVCs) and the presence of non-sustained ventricular tachycardia (NSVT, &amp;gt;3 PVCs with a rate &amp;gt;100 bpm). Frequent PVCs were defined as the presence of at least 30 PVCs per hour. We also collected clinical and echocardiographic findings for each patient. Assessment of clinical events at follow-up was performed by clinical visits or telephone interviews of patients or relatives (in case of fatal events). The primary endpoint of the study was the occurrence of cardiovascular events (CVE), a composite of cardiovascular death and resuscitation from cardiac arrest. All-cause-mortality was assessed as secondary endpoint. Survival Cox regression was applied to assess the univariate and multivariate association of clinical, echocardiographic and HM variables with endpoints. Results Clinical outcome could be obtained for 228 patients (85%), for an average follow-up of 3.5 years (range 1.0-8.6). Among these patients, frequent PVCs (≥30/hour) and episodes of NSVT at HM were found in 47 (20.6%) and 52 (22.4%) patients, respectively. CVE occurred in 26 patients (11.4%) and 63 patients died (27.6%). Frequent PVCs at HM were detected in 12 patients with (46.2%) and 35 patients without (17.3%) CVE (HR 2.29; 95% CI 1.03-5.09; p=0.04). One or more episodes of NSVT were detected in 9 patients with (34.6%) and 43 patients without (21.3%) CVE (HR 2.29; 95% CI 1.03-5.09; p=0.04), although it was not predictive of all-cause mortality (HR 1.18; 95% CI 0.48-2.77; p=0.52). Both the presence of PVCs&amp;gt;30/hour (HR 1.19; 95% CI 0.69-2.08; p=0.53) and NSVT (HR 0.93; 95% CI 0.52-1.65; p=0.22) were not significantly associated with all-cause mortality. Moreover, no clinical (age, gender, cardiovascular risk factors) and echocardiographic (aortic valve area, trans-aortic mean gradient, left ventricle mass and ejection fraction) variable showed significant association with both the primary and secondary outcome in our patients. Conclusions In our study the detection of frequent PVCs at HM after TAVI was a major predictor of CVE (cardiovascular death/cardiac arrest), suggesting that a 24-hour HM after TAVI can be helpful for risk stratification of these patients.

Relationship between premature ventricular complexes and stroke mortality in the general population

ObjectivesPredictors for increased stroke mortality identify those who may need closer monitoring and better hospital care. While the link between premature ventricular complexes (PVCs) and incident ischemic stroke has been reported, studies on the association with fatal stroke are non-existent. Materials and methodsWe examined the association of PVCs with stroke mortality in 8047 participants (56.5 ± 0.39 years, 53% women, 80.9% Non-Hispanic Whites) without prior history of stroke from the Third National Health and Nutrition Examination Survey. National Death Index was used to identify the date and cause of death. PVCs were detected from 12‑lead standard electrocardiograms. Cox proportional hazard analysis was used to examine the association between any PVC with stroke mortality. ResultsApproximately 2.1% (n = 134) participants had PVCs at baseline. Over a median follow-up of 22 years, 337 fatal strokes occurred. More strokes occurred in participants with baseline PVCs compared to those without (unadjusted cumulative incidence of stroke 9.5% vs. 2.5% respectively, p-value 0.001). In a multivariable-adjusted model, the presence of PVC was associated with an increased risk of stroke mortality (HR (95%CI): 2.50 (1.15–5.43). This association was stronger in participants with coronary heart disease (CHD) than those without it (HR (95%CI): 5.98 (2.2–16.2) vs. 1.97 (0.75–5.1) respectively; interaction-p = 0.008). ConclusionsPVCs are associated with an increased risk of stroke mortality, especially among individuals with CHD. Whether improved hospital care or modifying PVCs could change outcomes should be examined in prospective studies.

Sports Activity and Arrhythmic Risk in Cardiomyopathies and Channelopathies: A Critical Review of European Guidelines on Sports Cardiology in Patients with Cardiovascular Diseases.

The prediction and prevention of sudden cardiac death is the philosopher’s stone of clinical cardiac electrophysiology. Sports can act as triggers of fatal arrhythmias and therefore it is essential to promptly frame the athlete at risk and to carefully evaluate the suitability for both competitive and recreational sports activity. A history of syncope or palpitations, the presence of premature ventricular complexes or more complex arrhythmias, a reduced left ventricular systolic function, or the presence of known or familiar heart disease should prompt a thorough evaluation with second level examinations. In this regard, cardiac magnetic resonance and electrophysiological study play important roles in the diagnostic work-up. The role of genetics is increasing both in cardiomyopathies and in channelopathies, and a careful evaluation must be focused on genotype positive/phenotype negative subjects. In addition to being a trigger for fatal arrhythmias in certain cardiomyopathies, sports also play a role in the progression of the disease itself, especially in the case arrhythmogenic right ventricular cardiomyopathy. In this paper, we review the latest European guidelines on sport cardiology in patients with cardiovascular diseases, focusing on arrhythmic risk stratification and the management of cardiomyopathies and channelopathies.

Smartwatches may Underdetect Pulse in the Presence of Premature Ventricular Complexes

Recent trials have brought the potential role of smartwatches in pulse rate and arrhythmia monitoring to public attention, potentially leading to the misconception that the technology provides information of diagnostic quality. While some can record single-lead electrograms, most owned by the general public utilise photoplethysmography (PPG) to measure pulse rates. In the presence of arrhythmias causing reduced left ventricular output, PPG may under-detect pulse; analogous to an apical–radial deficit.

Premature ventricular complexes on screening electrocardiogram and risk of ischemic stroke.

Premature ventricular complexes (PVCs) detected from long-term ECG recordings have been associated with an increased risk of ischemic stroke. Whether PVCs seen on routine ECG, commonly used in clinical practice, are associated with an increased risk of ischemic stroke remains unstudied. This analysis included 24 460 participants (aged, 64.5+9.3 years; 55.1% women; 40.0% blacks) from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study who were free of stroke at the time of enrollment. PVCs were ascertained from baseline ECG (2003-2007), and incident stroke cases through 2011 were confirmed by an adjudication committee. A total of 1415 (5.8%) participants had at least 1 PVC at baseline, and 591 developed incident ischemic stroke during an average (SD) follow-up of 6.0 (2.0) years. In a cox proportional hazards model adjusted for age, sex, race, geographic region, education, previous heart disease, systolic blood pressure, blood pressure-lowering medications, current smoking, diabetes mellitus, left ventricular hypertrophy by ECG, and aspirin use and warfarin use, the presence of PVCs was associated with 38% increased risk of ischemic stroke (hazard ratio [95% confidence interval], 1.38 [1.05-1.81]). PVCs are common on routine screening ECGs and are associated with an increased risk of ischemic stroke.

The role of aortic valve anatomy in determining the site of origin of ventricular ectopic beats: correlation between echocardiographic and electrophysiologic data

Purpose: In presence of premature ventricular complexes (PVCs) arising from both Ventricular Outflow Tracts (RVOT and LVOT) it's often difficult to determine the origin before intracardiac mapping, due to smooth different ECG features for adiacent sites (posteroseptal RVOT, anteroseptal LVOT, Aortic Cusps). The aim of our study was to determine if the aortic valve anatomy as assessed by transthoracic echocardiography (TTE) is correlated with the origin site of the PVCs in patients with no evidence of Structural Heart Disease (SHD) and uncertain ECG features who undergo ablation with Radio-Frequency (RF) of monomorphic PVCs. Methods and materials: Thirty-one consecutive patients (mean age 52.5±18 yrs, 19 males) with no evidence of SHD who underwent RF ablation of PVCs were enrolled in our study. In all patients the 24 h Holter monitoring showed that at least 20% of the total heart beats was represented by monomorphic PVCs arising from RVOT or LVOT. Ablation was performed using electro-anatomic mapping and image-integration provided by intracardiac echo. The site of origin of the PVCs was determined according to the site of effective ablation. A complete standard TTE was performed before the ablation procedure, including an emphasized study of the aortic valve; aortic valve sclerosis (AVS) was defined by the presence of enhanced echogenicity/thickness (>2mm) of the aortic cuspids or the presence of focal calcifications. Results: The systolic left ventricular function expressed as ejection fraction (%) was normal in all patients (58.5±7.2). AVS was found in 11 pts, in 10 being associated with trivial valvular regurgitation. The ablation procedure was acutely successful in all patients. PVCs were originating from the LVOT in 12 pts (38%). All patients with PVCs originating from RVOT had normal aortic valve, instead AVS was present in 92% of patients with PVCs from LVOT and all 3 patients with PVCs from the Aortic Cusps. Conclusions: The presence of the aortic valve sclerosis assessed by transthoracic echocardiography was correlated with the LVOT origin of the premature ventricular complexes and it could help the preoperative management of the patients without structural heart disease who undergo RF ablation of monomorphic PVCs in presence of ambiguous ECG features.

Premature Ventricular Complexes and the Risk of Incident Stroke

Premature ventricular complexes (PVCs) on a 2-minute electrocardiogram are a common, largely asymptomatic finding associated with increased risk of coronary heart disease and death. They may reflect atherosclerosis or other pathogenic pathways that predispose to arrhythmias and stroke. We conducted a prospective evaluation of the Atherosclerosis Risk In Communities Study cohort (n=14,783) of middle-aged men and women to assess whether the presence of PVCs at study baseline (1987 to 1989) influenced the risk of incident stroke through December 31, 2004. PVCs were seen in 6.1% of the participants at baseline, and 729 (4.9%) had incident stroke. The unadjusted cumulative proportion of incident stroke in individuals with any PVC was 6.6% compared with 4.1% in those without PVC. The unadjusted hazard ratio of incident stroke in individuals with any PVC compared with those without any PVCs was 1.71 (95% CI, 1.33 to 2.20). Among individuals without hypertension and diabetes at baseline, PVCs were independently associated with incident stroke (hazard ratio: 1.72; 95% CI: 1.14 to 2.59). Among those with either diabetes or hypertension, the presence of any PVCs did not increase the risk of stroke. The association was stronger for noncarotid embolic stroke than for thrombotic stroke and its magnitude increased with higher frequency of PVCs. Frequent PVCs are associated with risk of incident stroke in participants free of hypertension and diabetes. This suggests that PVCs may contribute to atrioventricular remodeling or may be a risk marker for incident stroke, particularly embolic stroke.

‘Where There’s Smoke …’

See related article, pages 588–593. Premature ventricular complexes (PVCs) are easily recognized abnormalities on a 12-lead electrocardiogram or rhythm strip. During medical school and residency, it was a surprise and disappointment to learn that such an obvious abnormality was dismissed as a benign rhythm disturbance and was not indicative of serious disease. In this issue of Stroke, Agarwal and colleagues1 report that PVCs seen on a single baseline 2-minute rhythm strip were associated with an increased risk of incident stroke. These findings are reported in a large cohort (>14 000) of middle-aged (45 to 64 years) American men and women followed for 15 to 17 years in the Atherosclerosis Risk in Communities (ARIC) study. In the 6.1% with PVCs, the adjusted hazard ratio for stroke was 1.4 (95% CI, 1.08 to 1.80) and the adjusted hazard ratio for a combined end point of stroke and death was 1.62 (95% CI, 1.44 to 1.83). Increased stroke risk was observed irrespective of gender and race. There was a marked increase in stroke risk in those participants with ≥4 PVCs in a 2-minute recording. PVCs are suggested to be a “culprit arrhythmia”2 in the development of cardiomyopathy and are reported to predict a heightened risk of new-onset atrial fibrillation (AF)3 and cardiovascular death.4,5 An association of PVCs with stroke risk has been reported in an earlier smaller study cited by the ARIC investigators. In the large ARIC study, PVCs were associated with new-onset AF and death. Agarwal and colleagues1 identified apparent effect modification on stroke risk between established stroke risk factors and the …

Late sudden cardiac death in the follow-up of patients having a heart valve prosthesis

Eight hundred thirty-one patients with Björk-Shiley prostheses (341 aortic, 345 mitral, and 145 double) had a mean follow-up time of 68.2 months per patient. Of these, 24 (16% of all deaths) died suddenly: six of 42 with aortic valve replacement (14.3%), 12 of 56 with mitral valve replacement (21.4%), and six of 36 with double valve replacement (16.6%). This correlated with evidence of premature ventricular complexes detected in multiple routine 12-lead follow-up electrocardiograms (p less than 0.001 for simple aortic or mitral valve replacements and p less than 0.01 for combined aortic and mitral valve replacements). Premature ventricular complexes were significantly more frequent among those who died suddenly than among survivors and those who died of other causes (p less than 0.001 in both cases); there were no significant differences between the latter two groups. The actuarial risk of sudden death was significantly greater among those patients who had premature ventricular complexes than among those who did not have this disorder (p = 0.0002). We conclude that the presence of premature ventricular complexes, as an independent variable, was correlated with the risk of sudden death.