https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 Invasive Endotyping in Patients with Angina and No Obstructive Coronary Artery Disease: A Randomized Controlled Trial https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54421 Wed 28 Feb 2024 15:04:01 AEDT ]]> Myocardial Perfusion PET for the Detection and Reporting of Coronary Microvascular Dysfunction: A JACC: Cardiovascular Imaging Expert Panel Statement https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53319 Wed 22 Nov 2023 09:36:39 AEDT ]]> Fractional Flow Reserve-Guided Stent Optimisation in Focal and Diffuse Coronary Artery Disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52450 Wed 11 Oct 2023 15:02:08 AEDT ]]> Index of Microcirculatory Resistance to predict microvascular obstruction in STEMI: A systematic review and meta-analysis https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54417 Tue 27 Feb 2024 13:49:12 AEDT ]]> PCI in Management of Acute Type A Aortic Dissection Involving the Left Main Coronary Artery https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52867 Mon 30 Oct 2023 10:14:48 AEDT ]]> Bias and loss to follow-up in cardiovascular randomized trials: a systematic review https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38955 Mon 29 Jan 2024 17:47:53 AEDT ]]> Assessment of vascular dysfunction in patients without obstructive coronary artery disease: why, how, and when https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38385 Mon 29 Jan 2024 17:45:25 AEDT ]]> Coronary perforation incidence, outcomes and temporal trends (COPIT): A systematic review and meta-analysis https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52299 Mon 09 Oct 2023 10:19:06 AEDT ]]> Coronary Artery Perforations: Glasgow Natural History Study of Covered Stent Coronary Interventions (GNOCCI) Study https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52298 Mon 09 Oct 2023 10:11:19 AEDT ]]> Comparative study of costs and resource utilization of rotational atherectomy versus intravascular lithotripsy for percutaneous coronary intervention https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47260 Mon 09 Jan 2023 12:57:32 AEDT ]]> Targeted Therapies for Microvascular Disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53867 Fri 19 Jan 2024 12:39:36 AEDT ]]> Targeted Therapies for Microvascular Disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53868 Fri 19 Jan 2024 12:38:51 AEDT ]]> Genetic dysregulation of endothelin-1 is implicated in coronary microvascular dysfunction https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39991 P = 0.013]. The G allele was associated with higher plasma serum ET-1 [least squares mean 1.59 pg/mL vs. 1.28 pg/mL; 95% confidence interval (CI) 0.10–0.53; P = 0.005]. Patients with rs9349379-G allele had over double the odds of CMD [odds ratio (OR) 2.33, 95% CI 1.10–4.96; P = 0.027]. Multimodality non-invasive testing confirmed the G allele was associated with linked impairments in myocardial perfusion on stress cardiac magnetic resonance imaging at 1.5 T (N = 107; GG 56%, AG 43%, AA 31%, P = 0.042) and exercise testing (N = 87; −3.0 units in Duke Exercise Treadmill Score; −5.8 to −0.1; P = 0.045). Endothelin-1 related vascular mechanisms were assessed ex vivo using wire myography with endothelin A receptor (ET_A) antagonists including zibotentan. Subjects with rs9349379-G allele had preserved peripheral small vessel reactivity to ET-1 with high affinity of ET_A antagonists. Zibotentan reversed ET-1-induced vasoconstriction independently of G allele status. Conclusion: We identify a novel genetic risk locus for CMD. These findings implicate ET-1 dysregulation and support the possibility of precision medicine using genetics to target oral ET_A antagonist therapy in patients with microvascular angina. Trial registration: ClinicalTrials.gov: NCT03193294.]]> Fri 15 Jul 2022 10:14:01 AEST ]]> Risk Stratification Guided by the Index of Microcirculatory Resistance and Left Ventricular End-Diastolic Pressure in Acute Myocardial Infarction https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49428 32) and LVEDP (>18 mm Hg) were predefined. Contrast-enhanced cardiovascular magnetic resonance imaging (1.5 Tesla) was acquired 2 to 7 days and 3 months postmyocardial infarction. The primary end point was major adverse cardiac events, defined as cardiac death/nonfatal myocardial infarction/heart failure hospitalization at 1 year. Results: IMR and LVEDP were both measured in 131 patients (mean age 59±10.7 years, 103 [78.6%] male, 48 [36.6%] with anterior myocardial infarction). The median IMR was 29 (interquartile range, 17–55), the median LVEDP was 17 mm Hg (interquartile range, 12–21), and the correlation between them was not statistically significant (r=0.15; P=0.087). Fifty-three patients (40%) had low IMR (≤32) and low LVEDP (≤18), 18 (14%) had low IMR and high LVEDP, 31 (24%) had high IMR and low LVEDP, while 29 (22%) had high IMR and high LVEDP. Infarct size (% LV mass), LV ejection fraction, final myocardial perfusion grade ≤1, TIMI (Thrombolysis In Myocardial Infarction) flow grade ≤2, and coronary flow reserve were associated with LVEDP/IMR group, as was hospitalization for heart failure (n=18 events; P=0.045) and major adverse cardiac events (n=21 events; P=0.051). LVEDP>18 and IMR>32 combined was associated with major adverse cardiac events, independent of age, estimated glomerular filtration rate, and infarct-related artery (odds ratio, 5.80 [95% CI, 1.60–21.22] P=0.008). The net reclassification improvement for detecting major adverse cardiac events was 50.6% (95% CI, 2.7–98.2; P=0.033) when LVEDP>18 was added to IMR>32. Conclusions: IMR and LVEDP in combination have incremental value for risk stratification following primary percutaneous coronary intervention. Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT02257294.]]> Fri 12 May 2023 15:30:00 AEST ]]>