The aim of this study was to investigate the association between left ventricular remodeling, atrial fibrillation (AF), and the severity of ventricular tachycardia (VT) in patients with ventricular rhythm disturbances admitted in a level 3 facility of acute cardiac care. Material and Methods: The RHYTHM-ACC registry was a single-center observational study, including 150 consecutive patients with sustained or non-sustained ventricular tachycardia (sVT and nsVT, respectively) admitted in an intensive cardiac care unit (ICCU), separated in: group 1 - 29 patients (21.01%) with dilated cardiomyopathy (DCM), and group 2 - 109 patients (78.99%) with normal ventricular performance. We investigated the difference between clinical characteristics of patients with sVT versus those with nsVT in each study group, and the association between AF and different forms of ventricular arrhythmia in 38 (25.33%) patients with AF and 112 (74.66%) patients in sinus rhythm. Results: There were no significant differences between the study groups with respect to type of ventricular arrhythmia: sVT (46.87% vs. 36.44%, p = 0.2), nsVT (43.75% vs. 55.93%, p = 0.2), or ventricular fibrillation (VF) (9.37% vs. 7.62%, p = 0.7). However, patients with DCM presented a significantly higher incidence of AF (43.75% vs. 20.33%, p = 0.01) and bundle branch block (37.5% vs. 11.86%, p = 0.0007). VF occurred more frequently in patients with AF compared to those in sinus rhythm (18.42% vs. 4.46%, p = 0.006). Multivariate analysis identified the co-existence of AF (OR = 4.8, p = 0.01) and the presence of a bundle branch block (BBB) (OR = 3.9, p = 0.03) as the most powerful predictors for the degeneration of VT into VF in patients admitted with sVT or nsVT in an ICCU unit. Conclusions: In patients with any type of VT admitted in an ICCU, the presence of ventricular remodeling is associated with a higher incidence of AF and conduction abnormalities, but not with a more severe pattern of ventricular arrhythmia. At the same time, AF and BBB seem to represent the most powerful predictors for degeneration of VT into VF, independent of the type of VT.
Atrial fibrillation (AF) is an increasingly widespread healthcare problem. AF can frequently present as a complication in acute coronary syndromes (ACS), especially in ST-elevation acute myocardial infarction (AMI), in which case it is the most frequent supraventricular rhythm disturbance with an estimated incidence of 6.8-21%. The presence of AF in ACS heralds worse outcomes in comparison to subjects in sinus rhythm, and several studies have shown that in AMI patients, both new-onset and pre-existing AF are associated with a higher risk of major adverse cardiovascular and cerebrovascular events during hospitalization. The cause of newonset AF in AMI is multifactorial. Although still incompletely understood, the mechanisms involved in the development of AF in acute myocardial ischemic events include the neurohormonal activation of the sympathetic nervous system that accompanies the AMI, ischemic involvement of the atrial myocytes, ventricular dysfunction, and atrial overload. The identification of patients at risk for AF is of great significance as it may lead to prompt therapeutic interventions and closer follow-up, thus improving prognosis and decreasing cardiovascular and cerebrovascular events. The present manuscript aims to summarize the current research findings related to new-onset AF in AMI patients, as well as the predictors and prognostic impact of this comorbid association.
Background: The role of periplaque fat (PPF), as a fragment of the total epicardial adipose tissue, measured in the vicinity of a target coronary lesion, more specifically within the close proximity of a vulnerable plaque, has yet to be evaluated.
The study aimed to evaluate the interrelation between PPF and coronary plaque vulnerability in patients with stable coronary artery disease (CAD). Secondary objective: evaluation of the relationship between the total pericardial fat and markers for plaque vulnerability.
Materials and methods: We prospectively enrolled 77 patients with stable CAD, who underwent 128-multislice computed tomography coronary angiography (CTCA), and who presented minimum one lesion with >50% stenosis. CTCA analysis included measurements of: total pericardial fat and PPF volumes, coronary plaque characteristics, markers for plaque vulnerability – positive remodeling (PR), low attenuation plaque (LAP), spotty calcifications (SC,) napkin ring sign (NRS). Study subjects were divided into two categories: Group 1 – 1 marker of plaque vulnerability (n = 36, 46.75%) and Group 2 – ≥1 marker of vulnerability (n = 41, 53.25%).
Results: The mean age of the population was 61.77 ± 11.28 years, and 41 (53.24%) were males. The analysis of plaque characteristics showed that Group 2 presented significantly longer plaques (16.26 ± 4.605 mm vs. 19.09 ± 5.227 mm, p = 0.02), remodeling index (0.96 ± 0.20 vs. 1.18 ± 0.33, p = 0.0009), and vessel volume (p = 0.027), and more voluminous plaques (147.5 ± 71.74 mm3 vs. 207.7 ± 108.9 mm3, p = 0.006) compared to Group 1. Group 2 presented larger volumes of PPF (512.2 ± 289.9 mm3 vs. 710.9 ± 361.9 mm3, p = 0.01) and of thoracic fat volume (1,616 ± 614.8 mm3 vs. 2,000 ± 850.9 mm3, p = 0.02), compared to Group 1, but no differences were found regarding the total pericardial fat (p = 0.49). Patients with 3 or 4 vulnerability markers (VM) presented significantly larges PPF volumes compared to those with 1 or 2 VM, respectively (p = 0.008). There was a significant positive correlation between PPF volume and the non-calcified (r = 0.474, 95% CI 0.2797–0.6311, p <0.0001), lipid-rich (r = 0.316, 95% CI 0.099–0.504, p = 0.005), and fibro-fatty (r = 0.452, 95% CI 0.2541–0.6142, p <0.0001) volumes. The total pericardial fat was significantly correlated only with the volume of lipid-rich plaques (p = 0.02).
Conclusions: Periplaque fat volume was associated with a higher degree of coronary plaque vulnerability. PPF was correlated with lipid-rich, fibro-fatty, and non-calcified plaque-related volumes, as markers for enhanced plaque vulnerability. PPF volume, assessed with native cardiac computed tomography, could become a novel marker for coronary plaque vulnerability.
The significant raise in the number of patients surviving an acute myocardial infarction (AMI) has increased the burden of morbidity and disability due to acute coronary events. This has led to an increasing awareness on the need to develop specific rehabilitation programs, both during the acute phase, as well as in out-patient settings. In the pre-revascularization era, AMI was treated in bed. Regardless of the known therapeutic benefits of bed rest, there are scarce data regarding a standardized protocol for the early rehabilitation of patients with AMI. An extensive group of AMI patients are still exposed to prolonged immobilization, with current data showing a disparity in the length of post-MI bed rest, with a time of immobilization reported to be from 2 to 12 days and 2 to 28 days. The growing body of evidence on the effects of early cardiac rehabilitation programs following an AMI suggests that early mobilization after the index event could improve the inflammatory response and further modulate the ventricular remodeling process. The timing, duration, and intensity of cardiac mobilization has not yet been established, and further research on the effects of mobilization as early as the first 12 to 24 hours after the acute event could be beneficial for both short- and long-term outcomes, inflammation, and ventricular remodeling with subsequent heart failure.
Background: Little is known on the effect of epicardial fat in pulmonary arterial hypertension (PAH). Therefore, the present study sought to perform a comparative analysis on the influence of epicar-dial fat thickness (EFT) on the right and left ventricular function, between three different etiological varieties of pulmonary arterial hypertension: caused by congenital heart defects (atrial septum defects with left to right shunt), by systemic sclerosis, and by myocardial ischemia.
Materials and Methods: This is a prospective observational study on
50 patients with documented PAH (systolic pulmonary artery pressure – PASP of >35 mmHg). The thickness of the epicardial adipose tissue was evaluated by 2D cardiac ultrasound, on the free wall of the right ventricle, during end-diastole, in the long parasternal axis view. The patients were divided into three study groups: Group 1 – PAH determined by congenital heart defects with left to right shunts (atrial septum defects, n = 25); Group 2 – PAH induced by systemic sclerosis (n = 12); Group 3 – PAH induced by myocardial ischemia (n = 13).
Results: The average age was 54.48 ± 10.78 years, 30% (n = 15) of subjects were males, with a mean body mass index of 24.65 ± 4.40 kg/m2, EFT was 9.15 ± 2.24 mm, and the PASP was 41.33 ± 5.11 mmHg. Patients in Group 3 were more likely to smoke (p = 0.025) and presented a significantly lower LVEF, compared to the other groups (Group 1: 60% ± 6 vs. Group 2: 60% ± 7 vs. Group 3: 48% ± 7, p <0.0001). The largest EFT was found in Group 3 (11.08 ± 2.39 mm), followed by Group 2 (9.14 ± 2.03 mm), and Group 1 (8.16 ± 1.57 mm) (p = 0.0003). The linear regression analysis found no significant correlations between EFT and other echocardiographic parameters: PASP (r = −0.228, p = 0.118), LVEF (r = −0.265, p = 0.06), TAPSW (r = 0.015, p = 0.912), TEI (r = 0.085, p = 0.552), RVEDD (r = −0.195, p = 0.173), RA area (r = −178, p = 0.214), and LA diameter (r = 0.065, p = 0.650).
Conclusions: Epicardial fat thickness was found to be significantly higher in patients with PAH induced by myocardial ischemia, followed by those with systemic sclerosis and congenital heart defects, respectively. EFT did not influence the echocardiographic parameters for left and right ventricular function in patients with pulmonary arterial hypertension of different etiologies.
Myocardial viability plays an important role in preventing the development of left ventricular remodeling following an acute myocardial infarction. A preserved viability in the infarcted area has been demonstrated to be associated with a lower amplitude of the remodeling process, while the extent of the non-viable myocardium is directly correlated with the amplitude of the remodeling process. A number of methods are currently in use for the quantification of the viable myocardium, and some of them are based on the estimation of myocardial perfusion during pharmacologic stress. 64-slice Multi-detector Computed Tomography (MDCT) during vasodilator stress test, associated with CT Coronary Angiography (CCTA) has a high diagnostic accuracy in evaluating myocardial perfusion. In this article, we present a sequence of 3 clinical cases that presented with symptoms of myocardial ischemia, who underwent 64-slice MDCT imaging at rest and during adenosine stress test, in order to assess the extent of the hypoperfused myocardial areas. Coronary artery anatomy and the Coronary Calcium Score was assessed for all 3 patients by performing CT Coronary Angiography. The combination of CT Angiography and adenosine stress CT myocardial perfusion imaging can accurately detect atherosclerosic lesions that cause perfusion abnormalities, compared with the combination of invasive angiography and single-photon emission computed tomography (SPECT).