Angiology

Ventricular arrest is a rare arrhythmic disease in the clinic; 35% to 55% of cases are associated with atrial fibrillation (AF). It is well known that ventricular arrest for ≥3 seconds can lead to brain symptoms such as dizziness and even syncope, but it is not clear whether ventricular pauses (≥3 seconds) with AF will lead to sudden cardiac death. If the implantation of a pacemaker can improve the quality of life of patients with permanent AF with ventricular arrest and whether it has a long-term protective effect on sudden cardiac death. To this end, we conducted a prospective follow-up observation study, which was conducted through telephone interviews and clinical hospital observation to obtain information on the quality of life, survival rate, and other details. The results show that for patients with permanent AF with ventricular arrest, pacemaker implantation cannot reduce sudden cardiac death, cardiovascular events, and stroke nor can it improve the cumulative survival rate. Fortunately, the implantation of pacemakers can improve the quality of life of patients.

We compared plaque characteristics between symptomatic and asymptomatic sides in patients with bilateral carotid vulnerable plaques using magnetic resonance imaging (MRI). Participants (n = 67; mean age: 65.8 ± 7.7 years, 61 males) with bilateral carotid vulnerable plaques were included. Vulnerable plaques were characterized by intraplaque hemorrhage (IPH), large lipid-rich necrotic core (LRNC), or fibrous cap rupture (FCR) on MRI. Symptomatic vulnerable plaques showed greater plaque burden, LRNC volume (median: 221.4 vs 134.8 mm³, P = .003), IPH volume (median: 32.2 vs 22.5 mm³, P = .030), maximum percentage (Max%) LRNC (median: 51.3% vs 41.8%, P = .002), Max%IPH (median: 13.4% vs 9.5%, P = .022), cumulative slices of LRNC (median: 10 vs 8, P = .005), and more juxtaluminal IPH and/or thrombus (29.9% vs 6.0%, P = .001) and FCR (37.3% vs 16.4%, P = .007) than asymptomatic ones. After adjusting for plaque burden, differences in juxtaluminal IPH and/or thrombus (odds ratio [OR]: 5.49, 95% CI: 1.61-18.75, P = .007) and FCR (OR: 2.90, 95% CI: 1.16-7.24, P = .022) between bilateral sides remained statistically significant. For patients with bilateral carotid vulnerable plaques, symptomatic plaques had greater burden, more juxtaluminal IPH and/or thrombus, and FCR compared with asymptomatic ones. The differences in juxtaluminal IPH and/or thrombus and FCR between bilateral sides were independent of plaque burden.

Data regarding angiographic characteristics, clinical profile, and inhospital outcomes of patients with coronavirus disease 2019 (COVID-19) referred for coronary angiography (CAG) are scarce. This is an observational study analyzing confirmed patients with COVID-19 referred for CAG from 10 European centers. We included 57 patients (mean age: 66 ± 15 years, 82% male) , of whom 18% had previous myocardial infarction (MI) and 29% had renal insufficiency and chronic pulmonary disease. ST-segment elevation myocardial infarction (STEMI) was the most frequent indication for CAG (58%). Coronavirus disease 2019 was confirmed after CAG in 86% and classified as mild in 49%, with 21% fully asymptomatic. A culprit lesion was identified in 79% and high thrombus burden in 42%; 7% had stent thrombosis. At 40 days follow-up, 16 (28%) patients experienced a major adverse cardiovascular event (MACE): 12 deaths (92% noncardiac), 1 MI, 2 stent thrombosis, and 1 stroke. In an European multicenter registry, patients with confirmed COVID-19 infection referred for CAG during the first wave of the severe acute respiratory syndrome coronavirus 2 pandemic presented mostly with STEMI and were predominantly males with comorbidities. Severity of COVID-19 was in general noncritical and 21% were asymptomatic at the time of CAG. Culprit coronary lesions with high thrombus burden were frequently identified, with a rate of stent thrombosis of 7%. The incidence of MACE at 40 days was high (28%), mostly due to noncardiac death.

The most common cause of complete atrioventricular block (CAVB) is age-related fibrotic degeneration and is referred to as primary idiopathic complete atrioventricular block (iCAVB). This study aims to investigate the relationship between iCAVB and arterial stiffness using the cardio-ankle vascular index (CAVI).

In this study, of 205 CAVB patients, 41 patients with iCAVB implanted with a dual-chamber permanent pacemaker and 40 age- and gender-matched controls were studied. Arterial stiffness was assessed by a VaSera VS-1000 CAVI instrument. The CAVI values of patients with iCAVB were significantly higher compared with the controls (9.63 ± 1.42 vs 8.57 ± 1.12, P < .001). Idiopathic complete atrioventricular block frequency was higher among patients with abnormal CAVI values than those with borderline and normal CAVI (P = .04). In multivariate analysis, only CAVI was an independent predictor of iCAVB after adjusting for other relevant factors (odds ratio, 2.575; 95% CI [1.390-4.770]; P = .003). The present study demonstrated that CAVI, as a marker of arterial stiffness, was increased among elderly patients with iCAVB. Thus, we provide a possible additional mechanism linking easily measured CAVI with iCAVB.

We evaluated the predictive value of admission systemic immune-inflammation index (SII) for the risk of contrast-induced nephropathy (CIN) in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). The neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and SII (platelet × NLR) levels were calculated in 1621 consecutive patients with STEMI. The relationship of these parameters with CIN development within 72 hours of pPCI was analyzed. Of the study population, 343 (21.1%) cases developed CIN. The frequency of CIN was 11.1% in the first SII quartile, 11.6% in the second SII quartile, 26.8% in the third SII quartile, and 35% in the fourth SII quartile, which differed significantly between groups (P < .01). Age, baseline glomerular filtration rate, contrast media volume, hypertension, C-reactive protein levels, and the quartiles of SII were independent predictors of CIN. Patients in the third SII quartile versus first SII quartile (OR: 2.906, 95% CI, 1.903-4.437; P < .001), and fourth SII quartile versus first SII quartile (OR: 4.168, 95% CI, 2.754-6.313; P < .001) had a significantly higher risk for CIN in the multivariable model. The SII may be a promising inflammatory parameter to predict CIN after pPCI.

In this study, we aimed to evaluate the predictive value of admission C-reactive protein/albumin ratio (CAR) for acute kidney injury (AKI) in cases with moderate to severe chronic kidney disease (CKD) not on dialysis who presented with non-ST-segment elevation myocardial infarction (NSTEMI) and underwent coronary angiography (CAG). This cross-sectional and observational study included 420 NSTEMI patients. The study population was categorized based on the CAR tertiles as groups T1, T2, and T3. The primary outcome of the study was AKI development; 92 (21.9%) cases developed AKI. The frequency of AKI was significantly higher in the T3 group compared with the T2 and T1 groups (34% vs 17% vs 14%, P < .001). Age, estimated glomerular filtration rate, contrast media volume, and CAR (odds ratio: 1.36; 95% CI: 1.17-1.57; P < .01) were significant predictors of AKI. In a receiver operating characteristic curve analysis, CAR levels >0.20 predicted AKI development with a sensitivity of 74% and a specificity of 45%. We observed that the CAR may be a promising inflammatory parameter for AKI in NSTEMI patients with moderate to severe CKD after CAG.

We investigated the predictors, aetiology and long-term outcomes of acute kidney injury (AKI) following urgent percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS). Acute kidney injury occurred in 198 (7.2%) of 2917 patients: 14.1% of AKI cases were attributed to cardiogenic shock and 5.1% were classified as atheroembolic renal disease (AERD). Significant risk factors for AKI included age (odds ratio [OR] 1.05, 95% confidence limits [CI] 1.03-1.06), diabetes (OR 1.73, 95% CI 1.20-2.47), hypertension (OR 1.43, 95% CI 1.03-2.00), heart failure (OR 3.01, 95% CI 1.58-5.57), femoral access (OR 1.50, 95% CI 1.03-2.15), cardiogenic shock (OR 2.03, 95% CI 1.19-3.37) and ST-elevation myocardial infarction (STEMI) (OR 3.89, 95% CI 2.80-5.47). One-year mortality after AERD was 44.4% and renal replacement therapy (RRT) requirement 22.2% (compared with mortality 33.3% and RRT requirement 7.4%, respectively, in all other AKI patients). Mortality at 1 year was associated with AKI (OR 4.33, 95% CI 2.89-6.43), age (OR 1.08, 95% CI 1.06-1.09), heart failure (OR 1.92, 95% CI 1.05-3.44), femoral access (OR 2.05, 95% CI 1.41-2.95) and cardiogenic shock (OR 3.63, 95% CI 2.26-5.77). Acute kidney injury after urgent PCI is strongly associated with worse outcomes. Atheroembolic renal disease has a poor outcome and a high likelihood of long-term RRT requirement.

The data with respect to stable coronary artery disease (SCAD) are mainly confined to main vessel disease. However, there is a lack of information and long-term outcomes regarding isolated side branch disease. This study aimed to evaluate long-term major adverse cardiac and cerebrovascular events (MACCEs) in patients with isolated side branch coronary artery disease (CAD). A total of 437 patients with isolated side branch SCAD were included. After a median follow-up of 38 months, the overall MACCE and all-cause mortality rates were 14.6% and 5.9%, respectively. Among angiographic features, 68.2% of patients had diagonal artery and 82.2% had ostial lesions. In 28.8% of patients, the vessel diameter was ≥2.75 mm. According to the American College of Cardiology lesion classification, 84.2% of patients had either class B or C lesions. Age, ostial lesions, glycated hemoglobin A1c, and neutrophil levels were independent predictors of MACCE. On the other hand, side branch location, vessel diameter, and lesion complexity did not affect outcomes. Clinical risk factors seem to have a greater impact on MACCE rather than lesion morphology. Therefore, the treatment of clinical risk factors is of paramount importance in these patients.

The 2-year clinical outcomes according to pre-percutaneous coronary intervention (PCI) thrombolysis in myocardial infarction (TIMI) flow grade and reperfusion timing were investigated in patients with non-ST-segment elevation myocardial infarction (NSTEMI) who received newer-generation drug-eluting stents. A total of 7506 NSTEMI patients were divided into 2 groups: early (PCI ≤ 24 hours: n = 6398; pre-PCI TIMI 0/1 [n = 2729], pre-PCI TIMI 2/3 [n = 3669]) and delayed (PCI > 24 hours: n = 1108; pre-PCI TIMI 0/1 [n = 428], pre-PCI TIMI 2/3 [n = 680]) invasive groups. Major adverse cardiac events were defined as all-cause death, recurrent myocardial infarction, or any repeat revascularization. All-cause death (P = 0.005 and 0.009, respectively) and cardiac death (P = .003 and 0.046, respectively) were significantly higher in pre-PCI TIMI 0/1 patients than in pre-PCI TIMI 2/3 patients both in the early and delayed invasive groups. In pre-PCI TIMI 0/1 patients, all-cause death rate was significantly higher in the delayed group (P = .023). In pre-PCI TIMI 2/3 patients, the clinical end point was similar between the 2 groups. An early invasive strategy is preferred to a delayed invasive strategy in reducing all-cause death in patients with pre-PCI TIMI 0/1. However, in patients with pre-PCI TIMI 2/3, both treatment strategies are acceptable.

We explored the effect of admission hyperglycemia (AH) on the Global Registry of Acute Coronary Events (GRACE) risk score and major adverse cardiovascular and cerebrovascular event (MACCE) incidence during 1-year follow-up in acute myocardial infarction (AMI) patients. In this retrospective observational study enrolling 1098 AMI patients, hyperglycemia was defined as blood glucose level ≥180 mg/dl at admission. Overall, 158 and 84 patients of 272 diabetic and 826 non-diabetic patients were diagnosed with AH, respectively. Glucose levels at admission were closely associated with the GRACE score in patients with/without diabetes. MACCEs occurred in 222 patients; patients with AH showed significantly higher MACCE incidence (28.1%). Multivariate Cox logistic regression analysis indicated that AH was an independent risk factor for 1-year MACCEs. Subgroup analysis demonstrated that hyperglycemia increases MACCE risk in non-diabetic patients but not in diabetic patients. The admission glucose level combined with GRACE risk score showed a certain predictive value for MACCE incidence according to ROC analysis (OR = 0.798, p < .001). AH was strongly associated with a higher GRACE risk score in ST-segment elevation myocardial infarction patients. Thus, AH was an independent risk factor and had a high predictive value for MACCE during 1-year follow-up after AMI.

We evaluated if admission glycosylated hemoglobin (HbA_1c) and fasting glucose levels are correlated with the severity of coronary artery disease (CAD) in non-ST-elevation myocardial infarction (NSTEMI), nondiabetic, patients. Coronary artery disease severity, according to the anatomical synergy between percutaneous coronary intervention (PCI) with taxus and cardiac surgery (SYNTAX) score 2 (SSII), was retrospectively evaluated in 359 nondiabetic patients hospitalized with NSTEMI who underwent coronary angiography. Glucose intolerance was assessed by serum fasting glucose and HbA_1c levels. We stratified patients according to tertiles of SSII (≤21.5, 21.5-30.6, and ≥30.6). These score ranges were defined as SSII low, SSII mid, and SSII high, respectively. The average age of the patients was 57.1 ± 10.9 years; 189 (52.1%) patients were males. The average fasting glucose was 114 ± 52 mg/dL, HbA_1c was 5.8% ± 0.9%, and SSII was 18.9 ± 10.3. A stronger correlation was found between HbA_1c and SSII than fasting glucose and SSII (r1 = 0.901, P < .001, r2 = 0.378, P < .001, respectively), and HbA_1c level and hypertension were independent risk factors for SSII high (odds ratio [OR]: 2.2 (95% CI: 0.5-9.0, P < .001; OR: 1.1 (1.0-1.3), P = .007, respectively). In conclusion, in nondiabetic patients with NSTEMI, HbA_1c levels correlated with CAD severity as measured by the SSII.