Ventricular ectopy from the non-coronary cusp: Pathophysiological and anatomical considerations.
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ABSTRACT:
SUBMITTER: Ioannidis P
PROVIDER: S-EPMC8263327 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundVentricular premature complexes (VPCs) occasionally originate from the aortic sinus of Valsalva. Because the anterior part of the left coronary cusp (LCC) and right coronary cusp (RCC) are connected through the ventricular musculature at their bases, VPCs are more common in the LCC and the RCC than in the non-coronary cusp (NCC). We herein report a case in which VPCs were successfully ablated from the NCC, which is considered rare.Case summaryA 30-year-old woman was admitted to our hospital for the ablation of VPCs, which comprised 43% of the total heart beats. The clinical VPCs had an inferior axis and left bundle branch block morphology with a precordial transition between V4 and V5. Three-dimensional mapping of the target VPCs indicated that the earliest activation site was RCC. After radiofrequency (RF) energy application at the RCC, VPCs were temporally suppressed but recurred after 24 min. Remapping of the recurrent VPCs revealed that the earliest activation site shifted from the RCC to the His region. To avoid the risk of atrioventricular block, RF energy was applied from the NCC, which resulted in successful elimination of the VPCs without any complications.DiscussionThe present case suggests that RF energy application from the NCC may be a safe and effective option for the ablation of VPCs with the earliest activation at the RCC and His region.
| S-EPMC9007433 | biostudies-literature
Project description:Aortic cusps originating arrhythmias are rare; they have special electrocardiogram features that help to locate the site of origin. We report on a 20-year-old male patient without structural heart disease presenting with accelerated idioventricular rhythm; electrocardiogram analysis was typical of left coronary cusp origin.
| S-EPMC3227424 | biostudies-literature
Project description:BACKGROUND:The left coronary cusp is an uncommon but well-known site for the ablation of idiopathic ventricular tachycardia (VT). Proximity to the left coronary ostium makes ablation of this arrhythmia challenging. Different power settings have been described by various operators. Our objective was to describe the outcomes with low power ablation. METHODS:Once mapping confirmed origin from the left coronary cusp, ablation was performed if the best site was situated at least 5 mm from the left coronary ostium. Ablation was started at 15 W and, if successful, was stopped after 30 s. When required, higher powers were used up to 30 W. RESULTS:Ten patients with VT or premature ventricular beats mapped to the left coronary cusp were included in the study. No ablation was performed in one patient because of proximity to the left coronary ostium. Successful ablation was performed in eight of the other nine patients with a mean power of 18.1 ± 5.3 W and duration of 42.2 ± 13.5 s. There were no complications. All the eight patients remained free of recurrence at 16.8 ± 16.5 months of follow-up. CONCLUSIONS:VT can be ablated from the left coronary cusp close to the left coronary ostium. Ablation with low power is effective in achieving immediate success which is also durable with time while avoiding complications.
| S-EPMC6309714 | biostudies-literature
Project description:We present a unique case study report of a male individual with a history of mild nonischaemic cardiomyopathy, with no ventricular ectopy, that at the age of 76 years sustained multiple concussions (i.e., mild traumatic brain injury) within a week of each other. Concussion symptoms included cognitive difficulties, "not feeling well," lethargy, fatigue, and signs of depression. He was later medically diagnosed with postconcussion syndrome. The patient, WJT, was referred for cardiac and neurological assessment. Structural neuroimaging of the brain (MRI) was unremarkable, but electrocardiography (ECG) assessments using a 24-hour Holter monitor revealed significant incidence of ventricular ectopy (9.4%; 9,350/99,836 beats) over a period of 5-6 months after injury and then a further increase in ventricular ectopy to 18% (15,968/88,189 beats) during the subsequent 3 months. The patient was then prescribed Amiodarone 200?mg, and his ventricular ectopy and concussion symptoms completely resolved simultaneously within days. To the authors' knowledge, our study is the first to show a direct link between observable and documented cardiac dysregulation and concussion symptomology. Our study has important implications for both cardiac patients and the patients that sustain a concussion, and if medically managed with appropriate pharmacological intervention, it can reverse ventricular ectopy and concussion symptomology. More research is warranted to investigate the mechanisms for this dramatic and remarkable change in cardiac and cerebral functions and to further explore the brain-heart interaction and the intricate autonomic interaction that exists between the extrinsic and intracardiac nervous systems.
| S-EPMC7292985 | biostudies-literature
Project description:Background Premature ventricular contractions (PVCs) predict heart failure and death. Data regarding modifiable risk factors for PVCs are scarce. Methods and Results We studied 1424 Cardiovascular Health Study participants randomly assigned to 24-hour Holter monitoring. Demographics, comorbidities, habits, and echocardiographic measurements were examined as predictors of PVC frequency and, among 845 participants, change in PVC frequency 5 years later. Participants exhibited a median of 0.6 (interquartile range, 0.1-7.1) PVCs per hour. Of the more directly modifiable characteristics and after multivariable adjustment, every SD increase in systolic blood pressure was associated with 9% more PVCs (95% confidence interval [CI], 2%-17%; P=0.01), regularly performing no or low-intensity exercise compared with more physical activity was associated with ≈15% more PVCs (95% CI, 3-25%; P=0.02), and those with a history of smoking exhibited an average of 18% more PVCs (95% CI, 3-36%; P=0.02) than did never smokers. After 5 years, PVC frequency increased from a median of 0.5 (IQR, 0.1-4.7) to 1.2 (IQR, 0.1-13.8) per hour ( P<0.0001). Directly modifiable predictors of 5-year increase in PVCs, described as the odds per each quintile increase in PVCs, included increased diastolic blood pressure (odds ratio per SD increase, 1.16; 95% CI, 1.02-1.31; P=0.02) and a history of smoking (OR, 1.31; 95% CI, 1.02-1.68; P=0.04). Conclusions Enhancing physical activity, smoking cessation, and aggressive control of blood pressure may represent fruitful strategies to mitigate PVC frequency and PVC-associated adverse outcomes.
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Project description:Left ventricular assist device (LVAD) is essential for patients with severe heart failure, but there is a risk of thrombus formation on the aortic root and cusps, leading to coronary artery occlusion. Even with the narrowing of the echo-window due to LVAD, careful observation of coronary flow by transthoracic echocardiography can evaluate the patency of coronary flow non-invasively and immediately.
| S-EPMC9883730 | biostudies-literature
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| S-EPMC8767176 | biostudies-literature
Project description:Studies of patients presenting for catheter ablation suggest that premature ventricular contractions (PVCs) are a modifiable risk factor for congestive heart failure (CHF). The relationship among PVC frequency, incident CHF, and mortality in the general population remains unknown.The goal of this study was to determine whether PVC frequency ascertained using a 24-h Holter monitor is a predictor of a decrease in the left ventricular ejection fraction (LVEF), incident CHF, and death in a population-based cohort.We studied 1,139 Cardiovascular Health Study (CHS) participants who were randomly assigned to 24-h ambulatory electrocardiography (Holter) monitoring and who had a normal LVEF and no history of CHF. PVC frequency was quantified using Holter studies, and LVEF was measured from baseline and 5-year echocardiograms. Participants were followed for incident CHF and death.Those in the upper quartile versus the lowest quartile of PVC frequency had a multivariable-adjusted, 3-fold greater odds of a 5-year decrease in LVEF (odds ratio [OR]: 3.10; 95% confidence interval [CI]: 1.42 to 6.77; p = 0.005), a 48% increased risk of incident CHF (HR: 1.48; 95% CI: 1.08 to 2.04; p = 0.02), and a 31% increased risk of death (HR: 1.31; 95% CI: 1.06 to 1.63; p = 0.01) during a median follow-up of >13 years. Similar statistically significant results were observed for PVCs analyzed as a continuous variable. The specificity for the 15-year risk of CHF exceeded 90% when PVCs included at least 0.7% of ventricular beats. The population-level risk for incident CHF attributed to PVCs was 8.1% (95% CI: 1.2% to 14.9%).In a population-based sample, a higher frequency of PVCs was associated with a decrease in LVEF, an increase in incident CHF, and increased mortality. Because of the capacity to prevent PVCs through medical or ablation therapy, PVCs may represent a modifiable risk factor for CHF and death.
| S-EPMC4499114 | biostudies-literature
Project description:Premature ventricular contractions (PVCs) commonly coexist with cardiomyopathy. Recently, PVCs have been identified as a possible cause of cardiomyopathy. We developed a PVC-induced cardiomyopathy animal model using a novel premature pacing algorithm to assess timeframe and reversibility of this cardiomyopathy and examine the associated histopathologic abnormalities.Thirteen mongrel dogs were implanted with a specially programmed pacemaker capable of simulating ventricular extrasystoles. Animals were randomly assigned to either 12 weeks of bigeminal PVCs (n = 7) or no PVCs (control, n = 6). Continuous 24-hour Holter monitoring corroborated ventricular bigeminy in the PVC group (PVC, 49.8% versus control, < 0.01%; P<0.0001). After 12 weeks, only the PVC group had cardiomyopathy, with a significant reduction in left ventricular ejection fraction (PVC, 39.7 ± 5.4% versus control, 60.7 ± 3.8%; P < 0.0001) and an increase in left ventricular end-systolic dimension (PVC, 33.3 ± 3.5 mm versus control, 23.7 ± 3.6 mm; P < 0.001). Ventricular effective refractory period showed a trend to prolong in the PVC group. PVC-induced cardiomyopathy was resolved within 2 to 4 weeks after discontinuation of PVCs. No inflammation, fibrosis, or changes in apoptosis and mitochondrial oxidative phosphorylation were observed with PVC-induced cardiomyopathy.This novel PVC animal model demonstrates that frequent PVCs alone can induce a reversible form of cardiomyopathy in otherwise structurally normal hearts. PVC-induced cardiomyopathy lacks gross histopathologic and mitochondrial abnormalities seen in other canine models of cardiomyopathy.
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