Clinical symptoms of stable ischaemic heart disease

ESC CardioMed ◽  
2018 ◽  
pp. 1339-1343
Author(s):  
Ulrich Fischer-Rasokat ◽  
Christian Hamm

Ischaemic heart disease (IHD) becomes symptomatic when myocardial demand exceeds blood supply. Myocardial ischaemia leads to a wide range of symptoms, including chest pain as well as diffuse, worrisome sensations, all of which can be summarized under the term ‘chest discomfort’. Cardiac chest discomfort may be characterized according to four attributes: character, location, duration, and association with provoking or relieving factors. Typical angina pectoris, with a very high probability of significant epicardial coronary stenosis, can be diagnosed if three pre-specified criteria are met, whereas atypical angina pectoris, with only a moderate probability of IHD, and non-anginal chest pain fulfil fewer of these criteria. Angina pectoris can be quantified according to the Canadian Cardiovascular Society classification, which is based on threshold activities of angina-limited physical exertion. Some patients with IHD do not complain of chest discomfort but report symptoms such as sweating, nausea, or dyspnoea that have been demonstrated to be early indicators of IHD, denoted here as ‘angina equivalents’. Patients who do not experience any symptoms at all although myocardial ischaemia is detected are said to have ‘silent’ ischaemia. Patients with chest pain or discomfort use certain uniform hand gestures to describe the localization and character of the pain; thus, body language may be complementary to diagnostic criteria for IHD. Women are more likely to present with atypical forms of chest discomfort, and IHD is diagnosed roughly 10 years later in women than in men. Careful interpretation of patients’ descriptions of their symptoms is crucial to correctly diagnosing IHD.

Author(s):  
Bernhard L Gerber ◽  
Mouaz H Al-Mallah ◽  
Joao AC Lima ◽  
Mohammad R Ostovaneh

Chronic ischaemic heart disease (IHD) is one of the most common cardiac conditions worldwide and is generally caused by the consequences of coronary atherosclerosis, including myocardial infarction. Clinical challenges in chronic IHD include detection of myocardial ischaemia in symptomatic patients with suspected coronary artery disease (CAD), evaluation of myocardial viability in patients with established IHD and poor left ventricular ejection fraction (LVEF) when revascularization is considered, as well as risk stratification and identification of patients with chronic IHD at high risk of complications. Cardiovascular magnetic resonance (CMR) can provide vital answers to all three of these challenges. Stress CMR is now increasingly used to detect ischaemia by means of vasodilator stress perfusion or dobutamine stress contractile reserve stress imaging. For viability assessment, late gadolinium enhancement is currently the method of choice to detect myocardial infarction, and low-dose dobutamine stress magnetic resonance can provide additional information to determine viability and guide therapy. Cardiovascular risk in patients with chronic IHD is mainly determined by left ventricular function, most commonly utilizing LVEF, as well as infarct size, infarct characteristics, and ischaemic burden, which can all be measured reliably with CMR. This chapter will review the role of CMR for the detection of myocardial ischaemia, viability, and risk.


Author(s):  
Anthea Hatfield

Cardiovascular disease is common and patients coming to recovery room with any of these common problems will need special care. The essential signs and symptoms of hypertension, cardiac failure, ischaemic heart disease, and valvular heart disease are outlined. The actions and side-effects of the drugs that these patients take to control their symptoms are described. Recognizing and treating hypotension and myocardial ischaemia are very important and relevant, and they are fully discussed in this chapter.


1995 ◽  
Vol 39 (8) ◽  
pp. 977-985 ◽  
Author(s):  
Rozalind TEW ◽  
Elspeth A. Guthrie ◽  
Francis H. Creed ◽  
Lawrence Cotter ◽  
Stephen Kisely ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-20
Author(s):  
Dong Yan ◽  
Li-li Zhao ◽  
Bo-wen Yue ◽  
Hui Qian ◽  
Zi-han Zhang ◽  
...  

Objective. Coronary heart disease (CHD) has been regarded as a serious and common disease in the modern society. This study aims to investigate the effect of Granule of BU-XIN RUAN-MAI (BXRM) on angina pectoris of coronary heart disease and to explore the molecular mechanisms underlying Granule of BU-XIN RUAN-MAI-mediated protective activity against this disease. Methods. The effects of Granule of BU-XIN RUAN-MAI on clinical symptoms of patients’ angina were indicated by hemorheology indicators including high shear of blood viscosity, low shear of blood viscosity, plasma viscosity, erythrocyte rigidity index, D-D dimer, fibrinogen content, and lipid content. The effects of Granule of BU-XIN RUAN-MAI on isoprenaline-induced myocardial cell injury were determined by conducting H&E staining and by performing ELISA to examine the serum content of MDA, SOD, Na+/K+-ATPase, cAMP, and the content of inflammatory factors in isoprenaline-induced rats. Meanwhile, western blot and real time PCR were used to determine the expression of genes involved in oxidation and energy metabolism, and real time PCR was also used for determination of miR-542-3p expression. Luciferase reporter assay was conducted to test the binding sites of miR-542-3p on GABARAP 3′UTR. The chemical compositions of Granule of BU-XIN RUAN-MAI were determined by liquid LC-QTOF-MS. Results. Granule of BU-XIN RUAN-MAI significantly attenuated the clinical symptoms of patients’ angina by improving the patients’ heart rate and by decreasing the level of hemorheology indicators and also by reducing the serum content of TC, TG, LDL, and elevated HDL content. H&E staining demonstrated that Granule of BU-XIN RUAN-MAI ameliorated the myocardial ischemia in a dose-dependent manner. Besides, Granule of BU-XIN RUAN-MAI downregulated serum MDA content and upregulated the content of SOD, Na+/K+-ATPase, and cAMP in isoprenaline-induced rats. Granule of BU-XIN RUAN-MAI significantly improved oxidation stress by increasing PPARα expression, and it inhibited inflammation by downregulating expression and contents of IL-6, IL-1β, and TNF-α. Then, Granule of BU-XIN RUAN-MAI-containing serum increased the SOD content, and reduced the MDA content in angiotensin II-stimulated HUVEC cells. The granule of BU-XIN RUAN-MAI-containing serum obviously downregulated protein expressions of P40phox, P47phox, and P67phox in plasma membrane, and it significantly increased protein levels of P40phox, P47phox, and P67phox in the cytoplasm of HUVEC cells. Furthermore, GABARAP was reduced in heart tissues of ISO-induced rats and in angiotensin II-stimulated cell lines, and GABARAP was required for the inhibitory activity of Granule of BU-XIN RUAN-MAI on oxidation and inflammation in vivo and in vivo. GABARAP could be upregulated by Granule of BU-XIN RUAN-MAI by inhibiting the expression of miR-542-3p, which may significantly enhance oxidation and inflammation by targeting GABARAP in cardiomyocytes. Moreover, the silencing of GABARAP could obviously reverse the granule of BU-XIN RUAN-MAI-mediated protective activity against coronary heart disease, and interfering GABARAP expression also could partly block the anti-miR-542-3p-controlled oxidation and inflammation in cardiomyocytes. Besides, salidroside, loganin, and polydatin were the main compounds of granules of BU-XIN RUAN-MAI. Conclusion. Granule of BU-XIN RUAN-MAI is an excellent prescription for treatment of coronary heart disease by suppressing inflammation and NAPDH-mediated oxidative stress. The miR-542-3p/GABARAP axis is required for Granule of BU-XIN RUAN-MAI, exhibiting its protective activity against the pectoris of coronary heart disease.


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