Evaluation of microcirculatory protection in percutaneous revascularisation: A stent implantation technique and device comparison.

BACKGROUND: Coronary microvascular dysfunction (CMD) after percutaneous coronary intervention (PCI) is prognostically important and may also be a cause of persistent angina. The stent balloon inflation technique or material properties may influence the degree of CMD post-PCI. METHODS: Thirty-six patients with stable angina attending for elective PCI were randomized to either slow drug eluting stent (DES) implantation technique (DES slow group): +2 atm. every 5 s., maintained for a further 30 s or a standard stent implantation technique (DES std group): rapid inflation and deflation. PressureWire X with thermodilution at rest and hyperemia and optical coherence tomography (OCT) were performed pre- and post-PCI. Combined primary endpoints were changes in index of microvascular resistance (delta IMR) and coronary flow reserve (delta CFR) following PCI. The secondary endpoints included differences in cardiac troponin I (delta cTnI) at 6 h post-PCI, Seattle angina questionnaire (SAQ) at 1, 3, 6, and 12 months and OCT measures of stent results immediately post-PCI and at 3 months. RESULTS: Both groups were well matched, with similar baseline characteristics and OCT-defined plaque characteristics. Delta IMR was significantly better in the DES slow PCI arm with a median difference of -4.14 (95% CI -10.49, -0.39, p = 0.04). Delta CFR was also numerically higher with a median difference of 0.47 (95% CI -0.52, 1.31, p = 0.46). This did not translate to improved delta median cTnI (1.5 (34.8) vs. 0 (27.5) ng/L, p = 0.75) or median SAQ score at 3 months, (85 (20) vs. 95 (17.5), p = 0.47). CONCLUSION: Slow stent implantation is associated with less CMD after elective PCI in patients with stable angina.

Coronary artery dissection following radiofrequency ablation for atrial fibrillation: Case report and review of the literature.

Coronary artery injury following catheter ablation for cardiac arrhythmias is very rare. We present a case of left circumflex (LCx) coronary artery dissection causing inferoposterior ST-elevation myocardial infarction following radiofrequency (RF) ablation for atrial fibrillation (AF) in a 39-year-old male with no cardiovascular risk factors. This was confirmed on coronary angiography and intracoronary vascular ultrasound (IVUS). The likely etiology is thermal injury during RF ablation for AF, due to the close proximity of the left atrial appendage and left pulmonary veins to the LCx. He was successfully treated with primary percutaneous coronary intervention with good outcome. This is, to our knowledge, the first reported case of proven acute coronary dissection secondary to RF ablation for AF reported in the literature, and highlights the importance of considering this as a mechanism for coronary occlusion in these patients.

GLP-1 vasodilatation in humans with coronary artery disease is not adenosine mediated.

BACKGROUND: Incretin therapies appear to provide cardioprotection and improve cardiovascular outcomes in patients with diabetes, but the mechanism of this effect remains elusive. We have previously shown that glucagon-like peptide (GLP)-1 is a coronary vasodilator and we sought to investigate if this is an adenosine-mediated effect. METHODS: We recruited 41 patients having percutaneous coronary intervention (PCI) for stable angina and allocated them into four groups administering a specific study-related infusion following successful PCI: GLP-1 infusion (Group G) (n = 10); Placebo, normal saline infusion (Group P) (n = 11); GLP-1 + Theophylline infusion (Group GT) (n = 10); and Theophylline infusion (Group T) (n = 10). A pressure wire assessment of coronary distal pressure and flow velocity (thermodilution transit time-Tmn) at rest and hyperaemia was performed after PCI and repeated following the study infusion to derive basal and index of microvascular resistance (BMR and IMR). RESULTS: There were no significant differences in the demographics of patients recruited to our study. Most of the patients were not diabetic. GLP-1 caused significant reduction of resting Tmn that was not attenuated by theophylline: mean delta Tmn (SD) group G - 0.23 s (0.27) versus group GT - 0.18 s (0.37), p = 0.65. Theophylline alone (group T) did not significantly alter resting flow velocity compared to group GT: delta Tmn in group T 0.04 s (0.15), p = 0.30. The resulting decrease in BMR observed in group G persisted in group GT: - 20.83 mmHg s (24.54 vs. - 21.20 mmHg s (30.41), p = 0.97. GLP-1 did not increase circulating adenosine levels in group GT more than group T: delta median adenosine - 2.0 ng/ml (- 117.1, 14.8) versus - 0.5 ng/ml (- 19.6, 9.4); p = 0.60. CONCLUSION: The vasodilatory effect of GLP-1 is not abolished by theophylline and GLP-1 does not increase adenosine levels, indicating an adenosine-independent mechanism of GLP-1 coronary vasodilatation. TRIAL REGISTRATION: The local research ethics committee approved the study (National Research Ethics Service-NRES Committee, East of England): REC reference 14/EE/0018. The study was performed according to institutional guidelines, was registered on http://www.clinicaltrials.gov (unique identifier: NCT03502083) and the study conformed to the principles outlined in the Declaration of Helsinki.

Transcatheter mitral valve intervention: an emerging treatment for mitral regurgitation.

Mitral regurgitation (MR) is a valvular heart disease associated with significant morbidity and mortality. Transcatheter mitral valve intervention (TMVI) repairs or replaces the mitral valve through small arterial and venous entry sites and so avoids risks associated with open heart surgery. Transcatheter devices targeting components of the mitral apparatus are being developed to repair or replace it. Numerous challenges remain including developing more adaptable devices and correction of multiple components of the mitral annulus to attain durable results. The mitral valve apparatus is a complex structure and understanding of the mechanisms of MR is essential in the development of TMVI. There will likely be a complementary role between surgery and TMVI in the near future.

Improving the echocardiographic assessment of pulmonary pressure using the tricuspid regurgitant signal-The "chin" vs the "beard".

AIM: Transthoracic echocardiography (TTE) is a fundamental investigation for the noninvasive assessment of pulmonary hemodynamics and right heart function. The aim of this study was to assess the correlation and agreement of Doppler calculation of right ventricular systolic pressure (RVSP) and pulmonary vascular resistance (PVR) using "chin" and "beard" measurements of tricuspid regurgitant velocity (TRVmax ), with invasive pulmonary artery systolic pressure (PASP) and PVR. METHODS: One hundred patients undergoing right heart catheterisation (RHC) and near simultaneous transthoracic echocardiography were studied. TRVmax was recorded for "chin" measurement (distinct peak TRVmax signal) and where available (63 patients), "beard" measurement (higher indistinct peak TRVmax signal). RESULTS: Measurable TRV signal was obtained in 96 patients. Mean RVSPchin 54.7 ± 22.7 mm Hg and RVSPbeard 68.6 = 23 ± 26.3 mm Hg (P < .001). There was strong correlation between both RVSPchin and RVSPbeard with invasive PASP (Pearson's r = .9, R2  = 0.82, P < .001 - r = .88, R = .78, P < .001, respectively.). Bland-Altman analysis for RVSPchin and RVSPbeard showed a mean bias of -0.5 mm Hg (95% limits of agreement -21.4 to 20.5 mm Hg) and -10.7 (95% LOA -35.5 to 14.2 mm Hg), respectively. Receiver operator characteristics of TRVmax "chin" and "beard" for diagnosis of pulmonary hypertension was assessed with optimal cut-offs being 2.8 m/s (sensitivity 93%, specificity 87%) and 3.2 m/s (sensitivity 91%, specificity 82%), respectively. There was similar correlation between PVRchin and PVRbeard (r = .87, R2  = 0.75, P < .001 and r = .86, R2  = 0.74, P < .001, respectively). At higher PVR, there was overestimation of calculated PVR using PVRbeard . CONCLUSION: The accuracy of noninvasive measurement of right heart pressures is increased using the "chin" in estimation of both RVSP and PVR.

Outcomes Following Melody Transcatheter Pulmonary Valve Implantation for Right Ventricular Outflow Tract Dysfunction in Repaired Congenital Heart Disease: First Reported Australian Single Centre Experience.

BACKGROUND: Transcatheter pulmonary valve implantation (TPVI) with the Melody® transcatheter pulmonary valve (TPV) has demonstrated good haemodynamic and clinical outcomes in the treatment of right ventricular outflow tract (RVOT) conduit dysfunction in patients with repaired congenital heart disease CHD. We present the first Australian single centre experience of patients treated with Melody TPV. METHOD: A prospective, observational registry was developed to monitor clinical and haemodynamic outcomes in patients with RVOT dysfunction treated with the Melody TPV (Medtronic Inc, Minneapolis, United States). RESULTS: Seventeen patients underwent TPVI with Melody TPV at The Prince Charles Hospital between January 2009 and February 2016 with a median (range) age of 34 (R: 15-60). Fifteen (88%) were NYHA Class 2 dyspnoea and 11 (59%) had corrected Tetralogy of Fallot. Indication for TPVI was stenosis in eight (47%), regurgitation in two (12%) and mixed dysfunction in seven (41%). Device implantation was successful in all patients. Peak RVOT gradient was significantly reduced and there was no significant regurgitation post procedure. There was one (6%) major procedural adverse event and two (12%) major adverse events at last recorded follow-up. There were no patient deaths. Follow-up cardiac magnetic resonance imaging revealed a significant reduction in indexed right ventricular end diastolic volume. CONCLUSION: This study confirms the safety and effectiveness of TPVI with Melody TPV for RVOT dysfunction in repaired CHD.

Coronary Flow Variations Following Percutaneous Coronary Intervention Affect Diastolic Nonhyperemic Pressure Ratios More Than the Whole Cycle Ratios.

Background Post-percutaneous coronary intervention (PCI) fractional flow reserve ≥0.90 is an accepted marker of procedural success, and a cutoff of ≥0.95 has recently been proposed for post-PCI instantaneous wave-free ratio. However, stability of nonhyperemic pressure ratios (NHPRs) post-PCI is not well characterized, and transient reactive submaximal hyperemia post-PCI may affect their precision. We performed this study to assess stability and reproducibility of NHPRs post-PCI. Methods and Results Fifty-seven patients (age, 63.77±10.67 years; men, 71%) underwent hemodynamic assessment immediately post-PCI and then after a recovery period of 10, 20, and 30 minutes and repeated at 3 months. Manual offline analysis was performed to derive resting and hyperemic pressure indexes (Pd/Pa resting pressure gradient, mathematically derived instantaneous wave-free ratio, resting full cycle ratio, and fractional flow reserve) and microcirculatory resistances (basal microvascular resistance and index of microvascular resistance). Transient submaximal hyperemia occurring post-PCI was demonstrated by longer thermodilution time at 30 minutes compared with immediately post-PCI; mean difference of thermodilution time was 0.17 seconds (95% CI, 0.07-0.26 seconds; P=0.04). Basal microcirculatory resistance was also higher at 30 minutes than immediately post-PCI; mean difference of basal microvascular resistance was 10.89 mm Hg.s (95% CI, 2.25-19.52 mm Hg.s; P=0.04). Despite this, group analysis confirmed no significant differences in the values of resting whole cycle pressure ratios (Pd/Pa and resting full cycle ratio) as well as diastolic pressure ratios (diastolic pressure ratio and mathematically derived instantaneous wave-free ratio). Whole cardiac cycle NHPRs demonstrated the best overall stability post-PCI, and 1 in 5 repeated diastolic NHPRs crossed the clinical decision threshold. Conclusions Whole cycle NHPRs demonstrate better reproducibility and clinical precision post-PCI than diastolic NHPRs, possibly because of less perturbation from predominantly diastolic reactive hyperemia and left ventricular stunning. Registration URL: https://clinicaltrials.gov/ct2/show/NCT03502083; Unique identifier: NCT03502083 and URL: https://clinicaltrials.gov/ct2/show/NCT03076476; Unique identifier: NCT03076476.

Patent Foramen Ovale Closure: State of the Art.

Patent foramen ovale (PFO) is a common abnormality affecting between 20% and 34% of the adult population. For most people, it is a benign finding; however, in some people, the PFO can open widely to enable paradoxical embolus to transit from the venous to arterial circulation, which is associated with stroke and systemic embolisation. Percutaneous closure of the PFO in patients with cryptogenic stroke has been undertaken for a number of years, and a number of purpose-specific septal occluders have been marketed. Recent randomised control trials have demonstrated that closure of PFO in patients with cryptogenic stroke is associated with reduced rates of recurrent stroke. After a brief overview of the anatomy of a PFO, this article considers the evidence for PFO closure in cryptogenic stroke. The article also addresses other potential indications for closure, including systemic arterial embolisation, decompression sickness, platypnoea-orthodeoxia syndrome and migraine with aura. The article lays out the pre-procedural investigations and preparation for the procedure. Finally, the article gives an overview of the procedure itself, including discussion of closure devices.

Predictors of significant coronary artery disease in atrial fibrillation: Are cardiac troponins a useful measure.

BACKGROUND: Cardiac Troponin I (cTnI) is frequently measured in patients presenting with symptomatic atrial fibrillation (AF). The significance of elevated cTnI levels in this patient cohort is unclear. We investigated the value of cTnI elevation in this setting and whether it is predictive for significant coronary artery disease (sCAD). METHODS: We conducted a retrospective, single-center, case-control study of 231 patients who presented with symptomatic AF to The Prince Charles Hospital emergency department, Brisbane, Australia between 2006 and 2014. Patients who underwent serial cTnI testing and assessment for CAD were included. Clinical variables that are known to predict CAD and could potentially predict cTnI elevation were collected. Binary logistic regression was performed to identify predictors of sCAD and cTnI elevation. RESULTS: Cardiac Troponin I elevation above standard cut off was not predictive for sCAD after adjustment for other predictors (OR 1.62, 95% CI 0.79-3.32. p=0.19). However, the highest cTnI concentration value (cTnI peak) was predictive for sCAD (OR 2.02, 95% CI 1.02-3.97, p=0.04). Dyspnea on presentation (OR 4.52, 95% CI 1.87-10.91, p=0.001), known coronary artery disease (OR 3.44, 95% CI 1.42-8.32, p=0.006), and ST depression on the initial electrocardiogram (OR 2.57, 95% CI 1.11-5.97, p=0.028) predicted sCAD in our cohort, while heart rate on initial presentation was inversely correlated with sCAD (OR 0.99, 95% CI 0.971-1.00, p=0.034). CONCLUSION: Troponin elevation is common in patients presenting to hospital with acute symptomatic AF and it is not a reliable indicator for underlying sCAD in this patient cohort. However, cTnI peak was a predictor of significant coronary artery disease.