China
Africa
Explore chapters and articles related to this topic
Heart Failure in Adult Congenital Heart Disease
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Andrew Constantine, Ana Barradas-Pires, Isma Rafiq, Justyna Rybicka, Michael A. Gatzoulis, Konstantinos Dimopoulos
The coronary circulation is typically “anomalous” in ccTGA and a reduced coronary reserve has been described, even in the absence of ischemic symptoms.41 The conduction system in ccTGA is also abnormal, with anterior displacement of the atrioventricular (AV) node and the His bundles, and a higher incidence of AV block and chronotropic incompetence. This limits the role of beta-blocker therapy.
Functions of the Cardiovascular System
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The driving pressure in the coronary circulation is aortic pressure, but this is affected by extravascular compression of vessels during ventricular contraction. This is especially important in the left ventricle: in early systole, blood flow in the vessels is reversed, and most of the flow to the left ventricle takes place during diastole. This effect is less important in the right ventricle, as the pressure developed by contraction (25 mmHg) is much lower. In diastole, there is no compression of coronary vessels. Coronary blood flow to the left ventricle is intermittent, being maximal in diastole but stopping in early systole. In contrast, right ventricular coronary blood flow is pulsatile and is slightly higher during systole. Systolic compression of the coronary vessels is greater in the endocardium of the left ventricular wall than in the epicardium. Normally, the lack of blood flow in the left ventricle wall during systole is made up by the high flow during diastole (Figure 23.5).
Natriuretic Peptides and Cardiac Function
Published in Malcolm J. Lewis, Ajay M. Shah, Endothelial Modulation of Cardiac Function, 2020
Kazuhiro Yamamoto, Margaret M. Redfield, John C. Burnett
The coronary circulation can alter cardiac function through the delivery of oxygen or via the physical effects of coronary tugor (Gilbert and Glantz, 1989). Thus, in this section, effects of natriuretic peptides on coronary circulation are discussed.
Angiography derived assessment of the coronary microcirculation: is it ready for prime time?
Published in Expert Review of Cardiovascular Therapy, 2022
Jinying Zhou, Yoshinobu Onuma, Scot Garg, Nozomi Kotoku, Shigetaka Kageyama, Shinichiro Masuda, Kai Ninomiya, Yunlong Huo, Johan H.C. Reiber, Shengxian Tu, Jan J. Piek, Javier Escaned, Divaka Perera, Christos Bourantas, Hongbing Yan, Patrick W. Serruys
Coronary artery disease (CAD) has long been recognized as a disease of the major epicardial vessels affecting the conductance of the coronary circulation, however, whilst this is amenable to mechanical revascularization, this ignores coronary microvascular dysfunction which is the actual cause of angina and ischemia in up to two-thirds of patients [1,2]. Of note, if only noninvasive ischemia testing is used in patients with symptoms and documented non-obstructive coronary arteries, a median of 30% of patients with the underlying microvascular disease will remain undiagnosed [2]. Epicardial coronary arteries contribute to minimal resistance to coronary flow (5–10%), whilst microcirculation constitutes the remaining 95%. Being essentially a “black hole’ for angiographers (Figure 1(a,b)), microvasculature remains challenging in terms of physiological assessment. Following technical advances in intra-coronary pressure and flow measurements, quantitative functional assessment of the coronary microcirculation has become feasible using methods such as combined pressure-velocity loops [3], the thermodilution-derived pressure wire-based index of microvascular resistance (IMR) [4] and Doppler pressure wire-based hyperemic microvascular resistance (HMR) [5]. However, these techniques have not been widely incorporated into routine practice due to technical challenges, procedural costs, increased procedure time, and the intolerance some patients have to hyperemia.
Angina due to coronary artery spasm (variant angina): diagnosis and intervention strategies
Published in Expert Review of Cardiovascular Therapy, 2021
Thanh Ha Nguyen, Gao-Jing Ong, Olivia C Girolamo, Viviane De Menezes Caceres’, Armin Muminovic, Yuliy Y Chirkov, John D Horowitz
Coronary angiography with or without provocative testing represents the ‘gold standard’ for the definitive diagnosis of CAS. Provocative testing is not necessary if CSFP is present, since this in itself provides a diagnosis, and is rarely performed if any high-grade fixed stenosis is present. In the context of clinical suspicion of a diagnosis of CAS, all ‘fixed’ stenoses should be subjected to intracoronary injections of NTG [51]. The main indication for provocative testing, therefore, is apparently normal coronary circulation in a patient with a high probability of CAS. The two most widely used agents remain ergonovine and ACh. Ergonovine is a potent vasoconstrictor via α-adrenoceptor and 5-HT2 receptor activation, and can be given either intravenously [52], or intra-coronary [53] during invasive coronary angiography to induce CAS. ACh is administered at increasing doses directly into the left or right coronary arteries [54]. It is also important to note that administration of ACh can lead to transient atrioventricular block or bradycardia, and therefore necessitates empirical placement of a temporary pacing wire in the right ventricle for the duration of the provocative test.
Fragmented QRS predicts reperfusion failure and in-hospital mortality in ST-Elevation myocardial infarction: a systematic review and meta-analysis
Published in Acta Cardiologica, 2020
Jakrin Kewcharoen, Angkawipa Trongtorsak, Veraprapas Kittipibul, Narut Prasitlumkum, Chanavuth Kanitsoraphan, Prapaipan Putthapiban, Poemlarp Mekraksakit, Robert J. Pattison, Pattara Rattanawong
Primary percutaneous coronary intervention (pPCI) and thrombolytic therapy have long been the cornerstones in the effective management of ST-segment elevation myocardial infarction (STEMI) [1,2]. Prompt restoration of coronary circulation by either means is essential in optimizing myocardial salvage and reducing mortality [3]. Nevertheless, successful reperfusion, as defined by ST-segment resolution on an electrocardiogram (ECG) ≥50–70% [4,5], is not always achieved. Wong et al. reported successful reperfusion rates of 63% in thrombolytic therapy and 81% in pPCI for STEMI [6]. Clinical characteristics including prolonged time from symptoms onset to pre-hospital ECG, prolonged door-to-needle time and door-to-balloon time, and diabetes mellitus have been found to be associated with unsuccessful reperfusion [7–9].