Higher power short duration vs. lower power longer duration posterior wall ablation for atrial fibrillation and oesophageal injury outcomes: a prospective multi-centre randomized controlled study (Hi-Lo HEAT trial).

AIMS: Radiofrequency (RF) ablation for pulmonary vein isolation (PVI) in atrial fibrillation (AF) is associated with the risk of oesophageal thermal injury (ETI). Higher power short duration (HPSD) ablation results in preferential local resistive heating over distal conductive heating. Although HPSD has become increasingly common, no randomized study has compared ETI risk with conventional lower power longer duration (LPLD) ablation. This study aims to compare HPSD vs. LPLD ablation on ETI risk. METHODS AND RESULTS: Eighty-eight patients were randomized 1:1 to HPSD or LPLD posterior wall (PW) ablation. Posterior wall ablation was 40 W (HPSD group) or 25 W (LPLD group), with target AI (ablation index) 400/LSI (lesion size index) 4. Anterior wall ablation was 40-50 W, with a target AI 500-550/LSI 5-5.5. Endoscopy was performed on Day 1. The primary endpoint was ETI incidence. The mean age was 61 ± 9 years (31% females). The incidence of ETI (superficial ulcers n = 4) was 4.5%, with equal occurrence in HPSD and LPLD (P = 1.0). There was no difference in the median value of maximal oesophageal temperature (HPSD 38.6°C vs. LPLD 38.7°C, P = 0.43), or the median number of lesions per patient with temperature rise above 39°C (HPSD 1.5 vs. LPLD 2, P = 0.93). Radiofrequency ablation time (23.8 vs. 29.7 min, P < 0.01), PVI duration (46.5 vs. 59 min, P = 0.01), and procedure duration (133 vs. 150 min, P = 0.05) were reduced in HPSD. After a median follow-up of 12 months, AF recurrence was lower in HPSD (15.9% vs. LPLD 34.1%; hazard ratio 0.42, log-rank P = 0.04). CONCLUSION: Higher power short duration ablation was associated with similarly low rates of ETI and shorter total/PVI RF ablation times when compared with LPLD ablation. Higher power short duration ablation is a safe and efficacious approach to PVI.

Aortic and Systemic Arterial Stiffness Responses to Acute Exercise in Patients With Small Abdominal Aortic Aneurysms.

OBJECTIVE/BACKGROUND: Elevated arterial stiffness is a characteristic of abdominal aortic aneurysm (AAA), and is associated with AAA growth and cardiovascular mortality. A bout of exercise transiently reduces aortic and systemic arterial stiffness in healthy adults. Whether the same response occurs in patients with AAA is unknown. The effect of moderate- and higher intensity exercise on arterial stiffness was assessed in patients with AAA and healthy adults. METHODS: Twenty-two men with small diameter AAAs (36 ± 5 mm; mean age 74 ± 6 years) and 22 healthy adults (mean age 72 ± 5 years) were included. Aortic stiffness was measured using carotid to femoral pulse wave velocity (PWV), and systemic arterial stiffness was estimated from the wave reflection magnitude (RM) and augmentation index (Alx75). Measurements were performed at rest and during 90 min of recovery following three separate test sessions in a randomised order: (i) moderate intensity continuous exercise; (ii) higher intensity interval exercise; or (iii) seated rest. RESULTS: At rest, PWV was higher in patients with AAA than in healthy adults (p < .001), while AIx75 and RM were similar between groups. No differences were observed between AAA patients and healthy adults in post-exercise aortic and systemic arterial stiffness after either exercise protocol. When assessed as the change from baseline (delta, Δ), post-exercise ΔAIx75 was not different to the seated rest protocol. Conversely, post-exercise ΔPWV and ΔRM were both lower at all time points than seated rest (p < .001). ΔPWV was lower immediately after higher intensity than after moderate intensity exercise (p = .015). CONCLUSION: High resting aortic stiffness in patients with AAA is not exacerbated after exercise. There was a similar post-exercise attenuation in arterial stiffness between patients with AAA and healthy adults compared with seated rest. This effect was most pronounced following higher intensity interval exercise, suggesting that this form of exercise may be a safe and effective adjunctive therapy for patients with small AAAs.

Leg blood flow and skeletal muscle microvascular perfusion responses to submaximal exercise in peripheral arterial disease.

Peripheral arterial disease (PAD) is characterized by stenosis and occlusion of the lower limb arteries. Although leg blood flow is limited in PAD, it remains unclear whether skeletal muscle microvascular perfusion is affected. We compared whole leg blood flow and calf muscle microvascular perfusion after cuff occlusion and submaximal leg exercise between patients with PAD ( n = 12, 69 ± 9 yr) and healthy age-matched control participants ( n = 12, 68 ± 7 yr). Microvascular blood flow (microvascular volume × flow velocity) of the medial gastrocnemius muscle was measured before and immediately after the following: 1) 5 min of thigh-cuff occlusion, and 2) a 5-min bout of intermittent isometric plantar-flexion exercise (400 N) using real-time contrast-enhanced ultrasound. Whole leg blood flow was measured after thigh-cuff occlusion and during submaximal plantar-flexion exercise using strain-gauge plethysmography. Postocclusion whole leg blood flow and calf muscle microvascular perfusion were lower in patients with PAD than control participants, and these parameters were strongly correlated ( r = 0.84, P < 0.01). During submaximal exercise, total whole leg blood flow and vascular conductance were not different between groups. There were also no group differences in postexercise calf muscle microvascular perfusion, although microvascular blood volume was higher in patients with PAD than control participants (12.41 ± 6.98 vs. 6.34 ± 4.98 arbitrary units, P = 0.03). This study demonstrates that the impaired muscle perfusion of patients with PAD during postocclusion hyperemia is strongly correlated with disease severity and is likely mainly determined by the limited conduit artery flow. In response to submaximal leg exercise, microvascular flow volume was elevated in patients with PAD, which may reflect a compensatory mechanism to maintain muscle perfusion and oxygen delivery during recovery from exercise. NEW & NOTEWORTHY This study suggests that peripheral arterial disease (PAD) has different effects on the microvascular perfusion responses to cuff occlusion and submaximal leg exercise. Patients with PAD have impaired microvascular perfusion after cuff occlusion, similar to that previously reported after maximal exercise. In response to submaximal exercise, however, the microvascular flow volume response was elevated in patients with PAD compared with control. This finding may reflect a compensatory mechanism to maintain perfusion and oxygen delivery during recovery from exercise.

Atrioventricular block masked by posteroseptal bypass tract located in coronary sinus aneurysm.

Atrial fibrillation with concurrent ventricular preexcitation identifies a high-risk arrhythmic substrate and usually results in catheter ablation of the atrioventricular bypass tract. Electrocardiography can only approximate the anatomical location of an accessory pathway. Here we report a case where a bypass tract was localised to a coronary sinus aneurysm and antegrade atrioventricular conduction masked underlying atrioventricular nodal block.

Insulin in Acute Coronary Syndrome: a Narrative Review with Contemporary Perspectives.

The role of insulin in the treatment of acute coronary syndrome (ACS) has been widely studied over the past 100 years. The current indication for its use in this context is the treatment of hyperglycemia, irrespective of diabetes, which is associated with adverse outcome. Initial theories proposed that glucose was beneficial in the context of myocardial ischemia and insulin was required to enable glucose cell uptake. However, studies testing this hypothesis with routine insulin administration during ACS have produced disappointing results and research interest has therefore declined. We propose that the less well known but important vasodilator effect of insulin has been overlooked by some of these studies and warrants further consideration. Previous reports have shown that hyperinsulinemic euglycaemia improves myocardial blood flow reserve. With this in mind, this review considers the role of insulin in the context of ACS from the perspective of a vasodilator rather than a metabolic modulator. We discuss the importance of time to treatment, dosage of insulin administered, problems with hypoglycaemia and insulin resistance, and how they may have affected the outcomes of the major trials. Finally, we propose new study designs that allow determination of the optimal vasodilator conditions for the use of insulin as adjunctive pharmacotherapy during myocardial ischaemia.

His bundle combined with deep septal left bundle branch area pacing for atrial fibrillation prior to atrioventricular node ablation.

Background: To mitigate the risk of dyssynchrony-induced cardiomyopathy, international guidelines advocate His bundle pacing (HBP) with a ventricular backup lead prior to atrioventricular node ablation in treatment-refractory atrial fibrillation and normal left ventricular ejection fraction. As a result of concerns with long-term pacing parameters associated with HBP, this case series reports an adopted strategy of HBP combined with deep septal left bundle branch area pacing (dsLBBAP) in this patient cohort, enabling intrapatient comparison of the two pacing methods. Methods and Results: Eight patients aged 72 ± 10 years (left ventricular ejection fraction 53 ± 4%) underwent successful combined HBP and dsLBBAP implant prior to AV node ablation. Intrinsic QRS duration was 118 ± 46 ms. When compared to dsLBBAP, HBP had lower sensed ventricular amplitude (2.4 ± 1.1 vs. 15 ± 5.3 V, p = .001) and lower lead impedance (522 ± 57 vs. 814 ± 171ohms, p = .02), but shorter paced QRS duration (101 ± 20 vs. 119 ± 17 ms, p = .02). HBP pacing threshold was 1.0 ± 0.6 V at 1 ms pulse width, and dsLBBAP pacing threshold was 0.5 ± 0.2 V at 0.4 ms pulse width. Five patients underwent cardiac CT showing adequate dsLBBAP ventricular septal penetration (8.6 ± 1.3 mm depth, 2.4 ± 0.5 mm distance from left ventricular septal wall). No complications occurred during a mean follow-up duration of 121 ± 92 days. Conclusions: Combined HBP and dsLBBAP pacing is a feasible approach as a pace and ablate strategy for atrial fibrillation refractory to medical therapy.

Pacemaker-induced ventricular fibrillation during radiofrequency catheter ablation for ventricular tachycardia.

Prior to ventricular tachycardia ablation, this patient's cardiac implantable electronic device (CIED) was temporarily programmed to backup pacing mode with tachycardia therapies disabled. During radiofrequency energy delivery, the patient developed ventricular fibrillation requiring emergent cardioversion. Electrogram interrogation showed that the CIED switched to noise reversion mode during ablation. The consequent asynchronous pacing resulted in a paced QRS landing on an intrinsic T wave, inducing ventricular fibrillation. This serves as an important reminder that asynchronous pacing consequent to CIED oversensing could occur in any procedure that could cause electromagnetic interference such as radiofrequency cathteter ablation.

Skeletal muscle microvascular perfusion responses to cuff occlusion and submaximal exercise assessed by contrast-enhanced ultrasound: The effect of age.

Impairments in skeletal muscle microvascular function are frequently reported in patients with various cardiometabolic conditions for which older age is a risk factor. Whether aging per se predisposes the skeletal muscle to microvascular dysfunction is unclear. We used contrast-enhanced ultrasound (CEU) to compare skeletal muscle microvascular perfusion responses to cuff occlusion and leg exercise between healthy young (n = 12, 26 ± 3 years) and older (n = 12, 68 ± 7 years) adults. Test-retest reliability of CEU perfusion parameters was also assessed. Microvascular perfusion (microvascular volume × flow velocity) of the medial gastrocnemius muscle was measured before and immediately after: (a) 5-min of thigh-cuff occlusion, and (b) 5-min of submaximal intermittent isometric plantar-flexion exercise (400 N) using CEU. Whole-leg blood flow was measured using strain-gauge plethysmography. Repeated measures were obtained with a 15-min interval, and averaged responses were used for comparisons between age groups. There were no differences in post-occlusion whole-leg blood flow and muscle microvascular perfusion between young and older participants (p > .05). Similarly, total whole-leg blood flow during exercise and post-exercise peak muscle microvascular perfusion did not differ between groups (p > .05). The overall level of agreement between the test-retest measures of calf muscle perfusion was excellent for measurements taken at rest (intraclass correlation coefficient [ICC] 0.85), and in response to cuff occlusion (ICC 0.89) and exercise (ICC 0.95). Our findings suggest that healthy aging does not affect muscle perfusion responses to cuff-occlusion and submaximal leg exercise. CEU muscle perfusion parameters measured in response to these provocation tests are highly reproducible in both young and older adults.

An Experimental Series Investigating the Effects of Hyperinsulinemic Euglycemia on Myocardial Blood Flow Reserve in Healthy Individuals and on Myocardial Perfusion Defect Size following ST-Segment Elevation Myocardial Infarction.

BACKGROUND: Incomplete restoration of myocardial blood flow (MBF) is reported in up to 30% of ST-segment elevation myocardial infarction (STEMI) despite prompt mechanical revascularization. Experimental hyperinsulinemic euglycemia (HE) increases MBF reserve (MBFR). If fully exploited, this effect may also improve MBF to ischemic myocardium. Using insulin-dextrose infusions to induce HE, we conducted four experiments to determine (1) how insulin infusion duration, dose, and presence of insulin resistance affect MBFR response; and (2) the effect of an insulin-dextrose infusion given immediately following revascularization of STEMI on myocardial perfusion. METHODS: The MBFR was determined using myocardial contrast echocardiography. Experiment 1 (insulin duration): 12 participants received an insulin-dextrose or saline infusion for 120 minutes. MBFR was measured at four time intervals during infusion. Experiment 2 (insulin dose): 22 participants received one of three insulin doses (0.5, 1.5, 3.0 mU/kg/minute) for 60 minutes. Baseline and 60-minute MBFRs were determined. Experiment 3 (insulin resistance): five metabolic syndrome and six type 2 diabetes (T2DM) participants received 1.5 mU/kg/minute of insulin-dextrose for 60 minutes. Baseline and 60-minute MBFRs were determined. Experiment 4 (STEMI): following revascularization for STEMI, 20 patients were randomized to receive either 1.5 mU/kg/minute insulin-dextrose infusion for 120 minutes or standard care. Myocardial contrast echocardiography was performed at four time intervals to quantify percentage contrast defect length. RESULTS: Experiment 1: MBFR increased with time through to 120 minutes in the insulin-dextrose group and did not change in controls. Experiment 2: compared with baseline, MBFR increased in the 1.5 (2.42 ± 0.39 to 3.25 ± 0.77, P = .002), did not change in the 0.5, and decreased in the 3.0 (2.64 ± 0.25 to 2.16 ± 0.33, P = .02) mU/kg/minute groups. Experiment 3: compared with baseline, MBFR increase was only borderline significant in metabolic syndrome and T2DM participants (1.98 ± 0.33 to 2.59 ± 0.45, P = .04, and 1.67 ± 0.35 to 2.14 ± 0.21, P = .05). Experiment 4: baseline percentage contrast defect length was similar in both groups but with insulin decreased with time and was significantly lower than in controls at 60 minutes (2.8 ± 5.7 vs 13.7 ± 10.6, P = .02). CONCLUSIONS: Presence of T2DM, insulin infusion duration, and dose are important determinants of the MBFR response to HE. When given immediately following revascularization for STEMI, insulin-dextrose reduces perfusion defect size at one hour. Hyperinsulinemic euglycemia may improve MBF following ischemia, but further studies are needed to clarify this.

Myocardial blood flow reserve is impaired in patients with aortic valve calcification and unobstructed epicardial coronary arteries.

BACKGROUND: Although calcific aortic valve disease (CAVD) is associated with coronary atherosclerosis, it is not known whether early CAVD is associated with coronary microcirculatory dysfunction (CMD). We sought to investigate the relationship between myocardial blood flow reserve (MBFR) - a measure of CMD, and early CAVD in the absence of obstructive epicardial coronary artery disease. We also determined whether this relationship was independent of coronary artery disease (CAD) and hs-CRP, a marker of systemic inflammation. METHODS: 183 patients with chest pain and unobstructed coronary arteries were studied. Aortic valve calcification score (AVCS), coronary total plaque length (TPL), and coronary calcium score were quantified from multislice CT. MBFR was assessed using vasodilator myocardial contrast echocardiography. Hs-CRP was measured from venous blood using a particle-enhanced immunoassay. RESULTS: Mean (±SD) participant age was 59.8 (9.6) years. Mean AVCS was 68 (258) AU, TPL was 15.6 (22.2) mm, and median coronary calcification score was 43.5AU. Mean MBFR was 2.20 (0.52). Mean hs-CRP was 2.52 (3.86) mg/l. Multivariable linear regression modelling incorporating demographics, coronary plaque characteristics, MBFR, and inflammatory markers, demonstrated that age (ß=0.05, 95% CI: 0.02, 0.08, P=0.007), hs-CRP (ß=0.09, CI: 0.02, 0.16, P=0.010) and diabetes (ß=1.03, CI: 0.08, 1.98, P=0.033), were positively associated with AVCS. MBFR (ß=-0.87, CI: -1.44, -0.30, P=0.003), BMI (ß=-0.11, CI: -0.21, -0.01, P=0.033), and LDL (ß=-0.32, CI: -0.61, -0.03, P=0.029) were negatively associated with AVCS. TPL and coronary calcium score were not independently associated with AVCS when included in the regression model. CONCLUSION: Coronary microvascular function as determined by measurement of myocardial blood flow reserve is independently associated with early CAVD. This effect is independent of the presence of coronary artery disease and also systemic inflammation.

Tachycardia-induced cardiomyopathy- a fully reversible phenomenon.

Tachycardia induced cardiomyopathy (TIC) is a rare but potentially reversible cause of heart failure. The case of a patient with severe tachycardiomyopathy who had a favorable outcome following treatment of tachyarrythmia is presented here.