Emerging Role of Renal Sympathetic Denervation as an Adjunct Therapy to Atrial Fibrillation Ablation.

The central anatomical locus in the context of atrial fibrillation (AF) ablation has been the pulmonary veins. Despite the attainment of a modest long-term success rate through pulmonary vein isolation (PVI), the pursuit of achieving a therapeutic efficacy nearing a definitive cure has spurred an investigation into alternative strategies and anatomical loci beyond the pulmonary veins. Despite extensive exploration, none of these alternative targets have succeeded in establishing themselves as routine ablation sites comparable to the pulmonary veins. Consequently, there exists an imperative for further inquiry and refinement of ablation strategies to propel advancements within the domain of AF ablation, thereby augmenting patient outcomes. Simultaneously, the examination of the autonomic system's role in AF pathophysiology introduces an additional ablation target aimed at rectifying sympathovagal imbalance. This discourse presents a contemporary review of renal denervation (RDN) as an emergent and auspicious technique poised to complement PVI, thereby contributing substantively to the augmentation of long-term success within the ambit of AF rhythm-control strategies.

Atrial Fibrillation Monitoring in Cryptogenic Stroke: the Gaps Between Evidence and Practice.

Identifying occult paroxysmal atrial fibrillation as the etiology of cryptogenic stroke has been a top research priority in the past decade. This is because prompt initiation of anticoagulation has significantly decreased subsequent stroke risk. Available evidence suggests that prolonged cardiac monitoring after stroke increases the likelihood of detecting atrial fibrillation. However, further research is required to fill in the gaps in regard to the optimal period of monitoring, candidates for monitoring, etc. Here, we review the current evidence supporting the use of prolonged monitoring for cryptogenic stroke patients and discuss the directions of future research.

Subclinical and clinical contrast-induced acute kidney injury: data from a novel blood marker for determining the risk of developing contrast-induced nephropathy (ENCINO), a prospective study.

OBJECTIVE: Neutrophil gelatinase-associated lipocalin (NGAL) is produced in response to tubular injury. Contrast-induced acute kidney injury (CI-AKI) is associated with adverse outcomes in chronic kidney disease (CKD) patients. We sought to characterize blood NGAL level and the degree of kidney injury in CKD patients who underwent coronary angiography. METHODS: This study was a prospective, blinded assessment of blood samples obtained from patients with estimated glomerular filtration rates (eGFRs) between 15 and 90 mL/min/1.73 m2 undergoing elective coronary angiography with iodinated contrast. Blood NGAL and serum creatinine were measured at baseline, 1, 2, 4, 6, 12, 24 and 48 h after contrast administration. RESULTS: A total of 63 subjects with a mean eGFR of 48.17±16.45 mL/min/1.73 m2 were enrolled. There was a graded increase in baseline NGAL levels across worsening stages of CKD (p=0.0001). Post-procedure NGAL increased from baseline in each stage of CKD. Eight (12.7%) patients were diagnosed with CI-AKI by diagnostic criteria of 2012 KDIGO definition of CI-AKI, and seven (11.1%) patients developed subclinical CI-AKI defined by a twofold or greater rise in NGAL. There was no relationship between baseline eGFR and diabetes on the composite outcome of subclinical and clinical CI-AKI. CONCLUSIONS: Baseline and post-procedure NGAL are progressively elevated according to the baseline stage of CKD. Using a twofold rise in NGAL, 46.7% of composite CI-AKI is detected and complements the 53.3% of cases identified using KDIGO criteria. Traditional risk predictors were not independently associated with this composite outcome.

Familial Hypertrophic Cardiomyopathy With Fasciculoventricular Accessory Pathway.

Hypertrophic cardiomyopathy (HCM) is a common but an underdiagnosed condition. Fasciculoventricular bypass tract (FVBT) is rare. Concomitant presence of both conditions is well described in Danon disease. We report a case of familial HCM with FVBT linked to a heterozygous pathogenic variant, c.655G>C (p.Val219Leu), in the cardiac myosin binding protein C3 (MYBPC3) gene. (Level of Difficulty: Advanced.).

Catheter ablation of premature ventricular contractions originating from kissing papillary muscles.

Very thick left ventricular papillary muscles (PAMs) may kiss each other and premature ventricular contractions (PVCs) can originate from the sides of the PAMs facing each other. In such a setting, mapping of those PVCs is confusing and rendering catheter ablation challenging.

Paraoxonase 1 polymorphisms as the risk factor of coronary heart disease in a Thai population.

OBJECTIVE: Two common polymorphisms of the paraoxonase (PON1) gene, L55M and Q192R, were proven to mitigate atherosclerosis pathogenesis by protecting lipoproteins against peroxidation. This study was to evaluate the associations between both PON1 gene polymorphisms in Thai hyperlipidaemia with and without coronary heart disease (CHD). METHODS: Both PON1 genotypes were determined using PCR-RFLP in 103 healthy control subjects, 103 primary hyperlipidaemia without history of such diseases and 106 angiographically documented CHD patients. RESULTS: The frequencies of PON1 192R allele and 192RR genotype were significantly higher in CHD patients than in normal control subjects (P = 0.009 and 0.037, respectively). The significantly higher frequencies of 55M allele and 55LM genotype were also observed in CHD patients (P = 0.037 and P = 0.034, respectively). The frequencies of both PON1 polymorphisms were not different in primary hyperlipidaemia as compared to the normal control subjects. The odds ratio (OR) of 192RR genotype and 192R allele for CHD were 2.84 (1.17-6.99, P = 0.011) and 1.70 (1.11-2.61, P = 0.009), respectively. The age-adjusted OR for CHD was 2.72 (1.25-5.94, P = 0.012). These frequencies of both PON1 alleles were similar to those seen in other Asian populations. CONCLUSIONS: The association between PON1 polymorphisms and CHD risk was demonstrated in aThai population. These new data underscore the essence of ethnic variations in the interpretation of CHD associated with PON1 polymorphism.

Anaphylaxis: a ten years inpatient retrospective study.

BACKGROUND: The actual incidence of anaphylaxis is unknown. Periodical study of the anaphylaxis in different countries will raise the awareness to improve further the prevention and care. METHODS: To investigate anaphylaxis among inpatients in the previous decade, we conducted a retrospective study of adult patients between 1992 and 2001 at a tertiary care center in Bangkok. RESULTS: Of 448,211 admissions, 80 events of anaphylaxis in 79 patients (0.017%) were found. The incidence had increased from 2.6 to 46 per 100,000 inpatients. Mean age +/- SD was 36 +/- 16 years-old, with an equal male:female ratio. Drugs, mainly antibiotics and nonsteroidal anti-inflammatory agents, (48%) and food (31%) were the most common causes. Over-the-counter medication and multiple drug use were responsible for up to a half of the unspecified drug causes. There was no fatality. 84% received epinephrine, but in only 7% it was given intramuscularly. Fifteen cases (20%) had a history of prior anaphylaxis, nonetheless only one had received prefilled epinephrine. CONCLUSIONS: The rise in the incidence of anaphylaxis over the two decades of the study period is alarming. Raising the awareness of anaphylaxis management among healthcare providers and the public is warranted.

Twenty-five-year-old woman with palpitations and hypertrophic cardiomyopathy.

CLINICAL INTRODUCTION: A 25-year-old woman with a diagnosis of hypertrophic cardiomyopathy (HCM) and pre-excitation on ECG presented with unexplained syncope and daily palpitation. Genetic testing was positive for lysosome-associated membrane protein 2 (LAMP2) mutation which confirmed the diagnosis of Danon disease. Her younger sister was diagnosed with a similar condition and received a defibrillator implantation. Her 12-lead ECG (figure 1) and a long strip tracing (figure 2) are shown below.Figure 112-lead ECG. QUESTION: Where is the location of the accessory pathway and what is the next appropriate management?Anteroseptal pathway and catheter ablationMid-septal pathway and pacemaker/defibrillator implantationRight lateral pathway and catheter ablationFasciculoventricular pathway and electrophysiological studyLeft lateral pathway and electrophysiological study.

Leadless solution for arrhythmia-related sudden unexpected death in epilepsy.

A leadless pacemaker is a recently approved pacing technology that helps mitigate lead-related complications, but it has several limitations. Careful candidate selection is needed. Here, we demonstrate leadless pacing as the solution for prolonged postictal bradycardia/asystole; there is no consensus regarding pacemaker implantation for seizure patients with such a risk of sudden cardiac death.

Successful treatment of a cardiac resynchronization therapy nonresponder by identifying lead malpositioning.

This case describes some of the commonly overlooked device-related issues in patients who have reportedly failed to respond to cardiac resynchronization therapy (CRT). The case demonstrates voltage-dependent right ventricular capture instead of right atrial capture by a subtly malpositioned right atrial lead. CRT therapy failed to improve symptoms of heart failure and the diagnosis of "CRT nonresponder" was made. With a detailed fact-finding approach, the mechanism behind this nonresponse was identified, and the outcome of CRT was significantly improved with rectification of the problems.

A flow cytometric analysis of the inhibition of platelet reactivity due to nitrite reduction by deoxygenated erythrocytes.

Nitric oxide (NO), a small gas molecule, has long been known to be a potent inhibitor of platelet function but the physiological and pathological implications of platelet inhibition by NO have not been well clarified. We recently showed that the addition of nitrite to platelet-rich plasma in the presence of erythrocytes could inhibit platelet aggregation and this inhibitory effect of nitrite + erythrocytes was enhanced by deoxygenation of erythrocytes as measured by P-selectin expression and cGMP production. In order to study the nitrite effect on platelets at different oxygen levels, we used the flow cytometric assays to detect platelet membrane surface markers upon activation. The P-selectin and activated gpIIb/IIIa expression on platelet membranes in response to ADP, collagen and thrombin stimulation was measured at various hematocrit and oxygen levels. Nitrite (0.1 to 1.0 µM) significantly decreased the percentage of these surface markers on the platelet membrane at the hematocrit values above 23% and oxygen levels lower than 49 mmHg. The inhibitory effect of nitrite was augmented by increasing hematocrit values and decreasing oxygen saturation. C-PTIO (an NO scavenger) prevented the platelet inhibition by nitrite + erythrocytes whereas the inhibitors of NO synthase and xanthine oxidoreductase had no effect. These results support the proposal that circulating nitrite decreases platelet reactivity in the presence of partially deoxygenated erythrocytes through its reduction to NO, which may also explain certain differences between arterial and venous thrombosis and support directly the role of deoxyhemoglobin in this process. We believe that our flow cytometric assays offer a possibility to identify the individual molecular process involved in these effects.

Urine catalytic iron and neutrophil gelatinase-associated lipocalin as companion early markers of acute kidney injury after cardiac surgery: a prospective pilot study.

BACKGROUND: Open heart surgery with cardiopulmonary bypass is recognized as a common cause of acute kidney injury (AKI). The conventional biomarker creatinine is not sensitive enough to detect AKI until a significant decline in renal filtration has occurred. Urine neutrophil gelatinase-associated lipocalin (NGAL), part of an acute response to the release of tissue iron from cells, is an early biomarker and a predictor of AKI in a variety of clinical settings. We sought to evaluate the relationship between urine catalytic iron (unbound iron) and NGAL over the course of AKI due to cardiac surgery. METHODS: FOURTEEN PATIENTS WHO UNDERWENT OPEN HEART SURGERY HAD THE FOLLOWING MEASURED: serum creatinine (0, 12, 24, 48 and 72 h postoperatively), urine NGAL and urine catalytic iron (0, 8, 24 and 48 h postoperatively). Urine NGAL and urine catalytic iron were quantified by immunoassay and bleomycin-detectable iron assay, respectively. AKI was defined by the Acute Kidney Injury Network (AKIN) criteria. RESULTS: Urine catalytic iron increased significantly (p < 0.05) within 8 h and peaked at 24 h postoperatively in patients who developed AKI (n = 8, baseline 101.96 ± 177.48, peak 226.35 ± 238.23 nmol/l, p = 0.006), but not in non-AKI patients (n = 6, baseline 131.08 ± 116.21, peak 163.99 ± 109.62 nmol/l, p = 0.380). Urine NGAL levels also peaked at 24 h with significant increase observed only in AKI patients: AKI - baseline 34.88 ± 26.47, peak 65.50 ± 27.03 ng/ml, p = 0.043; non-AKI - baseline 59.33 ± 31.72, peak 71.00 ± 31.76 ng/ml, p = 0.100. The correlation between baseline levels of urine catalytic iron and NGAL and peak levels of urine catalytic iron and NGAL was r = 0.86, p < 0.0001. CONCLUSION: Urine catalytic iron appears to rise and fall in concert with NGAL in patients undergoing cardiac surgery and may be indicative of early AKI. Future research into the role that catalytic iron plays in acute organ injury syndromes and its potential diagnostic and therapeutic implications is warranted.