Chronic ischaemic heart disease

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.

ESC CardioMed ◽  
2018 ◽  
pp. 2836-2840
Author(s):  
Martha Gulati

The more atypical presentation of women makes the diagnostic evaluation of symptomatic women challenging and results in more frequent referral for diagnostic testing to improve the precision of the ischaemic heart disease likelihood estimate. The classification of ischaemic heart disease and myocardial infarction has moved beyond the diagnosis of obstructive coronary artery disease and encompasses ischaemia that can occur in the presence and absence of obstructive coronary artery disease. Consideration of the different pathophysiology of ischaemia that may occur in women needs to be considered in the evaluation and treatment of ischaemic heart disease in women.


2015 ◽  
Vol 16 (suppl 2) ◽  
pp. S139-S141
Author(s):  
L Faber ◽  
K T Nel ◽  
D Trifunovic ◽  
S Rodero ◽  
S Rodero ◽  
...  

Blood ◽  
1982 ◽  
Vol 60 (3) ◽  
pp. 650-654
Author(s):  
AB Nichols ◽  
J Owen ◽  
KL Kaplan ◽  
RR Sciacca ◽  
PJ Cannon ◽  
...  

In vivo platelet alpha-granule release and fibrin I formation were measured in 82 patients with ischemic heart disease by radioimmunoassay of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A. The presence and extent of coronary artery disease were determined by coronary arteriography, and the extent of left ventricular regional dysfunction was assessed by contrast left ventriculography. In patients with abnormal coronary arteriograms without previous myocardial infarction, mean levels of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A were not elevated. In patients in whom myocardial infarction had occurred more than 6 mo previously, platelet factor 4 (8.3 ng/ml; p less than 0.01) and beta-thromboglobulin (33.2 ng/ml; p less than 0.001) levels were significantly elevated, but fibrinopeptide A levels were normal. Levels of platelet factor 4 and beta- thromboglobulin were unrelated to the extent of coronary artery disease. In the patients with prior infarction, beta-thromboglobulin correlated directly with extent of left ventricular regional dysfunction (r = 0.53; p less than 0.01) and inversely with ejection fraction (r = -056; p less than 0.05). In a small group of patients with left ventricular aneurysm, mean fibrinopeptide A levels were also elevated. We interpret these findings as indicating that platelet release in patients with ischemic heart disease results from platelet reaction with previously infarcted myocardium rather than with the atherosclerotic coronary arteries.


2021 ◽  
Vol 10 (7) ◽  
pp. 409-413
Author(s):  
Shivakumar B.G. ◽  
Shivakumar N ◽  
Siddharth Gosavi ◽  
Shashank Shastry

BACKGROUND The study was conducted in an attempt to correlate serum uric acid levels with Killip class i.e. severity of heart failure in patients with acute myocardial infarction and to assess any influence of serum uric acid levels on predicting prognosis in patients with acute myocardial infarction. Ischaemic heart disease, particularly acute myocardial infarction is one of the leading causes of death across the world accounting for 12.7 % of global mortality. Low and middle-income countries are facing 80 % of the global burden of ischaemic heart disease death. Since the pathophysiology of acute myocardial infarction is complicated, proper risk stratification is essential for appropriate management and better outcome. Serum uric acid levels (SUA) have been correlated with coronary artery calcification and atherosclerosis. High SUA levels also have been identified as a risk marker for cardiovascular disease development, progression and mortality. METHODS The study design was a one-year cross-sectional study. 100 patients admitted with acute myocardial infarction within one day of the start of symptoms in the Department of Cardiology & Medicine were included from September 2018 to September 2019. In this study, patients with known causes of elevated uric acid levels (chronic kidney disease, gout, haematological malignancy, hypothyroidism, metabolic syndrome, myeloproliferative disease, lymphoproliferative disease, drugs– pyrazinamide, diuretics, ethambutol, ethanol, malignancy, G6PD deficiency and psoriasis) were included. Patients on drugs which raise serum uric acid e.g., salicylates (2 gm / d, hydrochlorothiazide, pyrazinamide), and chronic alcoholics were not included. Patients were further subjected to investigations like serum uric acid, ECG, 2D echo and other routine investigations. Urine albumin levels, troponin I, chest x-ray, fundoscopy, and fasting lipid profile were done. Investigation reports were analysed with the clinical profile and the data was compiled and appropriate statistical test was applied. RESULTS There were more cases of myocardial infarction above 40 years as compared to below 40 years of age and males (69 %) were more as compared to females (31 %) with the commonest presentation as chest pain. Majority of the patients had inferior wall myocardial infarction (IWMI) (40 %) and most (91 %) of the patients had left ventricular (LV) dysfunction (mild, moderate and severe). More patients with Killip class III and IV had abnormal uric acid levels as compared to class I, and II. Among 27 patients who expired, 23 were in Killip class III and IV (13 in Killip class III and 10 in class IV) and the mean serum uric acid levels of expired patients were elevated on all the 3 days with maximum elevation on day 1. CONCLUSIONS Patients with higher Killip class had higher levels of serum uric acid in comparison to patients of lower Killip class. Serum uric acid level in association with Killip class is a good predictor of the severity of heart failure and short-term mortality after myocardial infarction.


Blood ◽  
1982 ◽  
Vol 60 (3) ◽  
pp. 650-654 ◽  
Author(s):  
AB Nichols ◽  
J Owen ◽  
KL Kaplan ◽  
RR Sciacca ◽  
PJ Cannon ◽  
...  

Abstract In vivo platelet alpha-granule release and fibrin I formation were measured in 82 patients with ischemic heart disease by radioimmunoassay of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A. The presence and extent of coronary artery disease were determined by coronary arteriography, and the extent of left ventricular regional dysfunction was assessed by contrast left ventriculography. In patients with abnormal coronary arteriograms without previous myocardial infarction, mean levels of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A were not elevated. In patients in whom myocardial infarction had occurred more than 6 mo previously, platelet factor 4 (8.3 ng/ml; p less than 0.01) and beta-thromboglobulin (33.2 ng/ml; p less than 0.001) levels were significantly elevated, but fibrinopeptide A levels were normal. Levels of platelet factor 4 and beta- thromboglobulin were unrelated to the extent of coronary artery disease. In the patients with prior infarction, beta-thromboglobulin correlated directly with extent of left ventricular regional dysfunction (r = 0.53; p less than 0.01) and inversely with ejection fraction (r = -056; p less than 0.05). In a small group of patients with left ventricular aneurysm, mean fibrinopeptide A levels were also elevated. We interpret these findings as indicating that platelet release in patients with ischemic heart disease results from platelet reaction with previously infarcted myocardium rather than with the atherosclerotic coronary arteries.


2006 ◽  
Vol 63 (3) ◽  
pp. 287-292
Author(s):  
Sonja Salinger ◽  
Miloje Tomasevic ◽  
Jozef Glasnovic ◽  
Svetlana Apostolovic ◽  
Milan Pavlovic ◽  
...  

Background/Aim. Chronotropic incompetence during exercise stress testing after acute myocardial infarction is an indicator of ischemia or impaired left ventricular function. On the other side, infusion of dobutamine leads to a typical dose-dependent increase in heart rate. The aim of this study was to evaluate of paradoxical sinus deceleration during dobutamine stress echocardiography (DSE), as the sign of ischemia and impaired left ventricular function, or the consequence of infarction localization, and the estimation of prognostic significance after acute myocardial infarction. Methods. Our investigation comprised 81 patients hospitalized because of the acute myocardial infarction, and all of them had uncomplicated infarction. Fifty five patients were treated with thrombolytic therapy (67.9%); 53 patients (65.4%) had anterior myocardial infarction, and 28 patients (34.6%) had inferoposterior localization of myocardial infarction. After 10-12 days all of them underwent dobutamine stress echocardiography examination. During the next 3-6 months, the patients underwent coronary angiography. The average follow-up period was 36?22 months. Results. A decrease in heart rate occurred at the dobutamine doses increasing from 15-40mcg/kg/min in 9 (11.1%) of the patients, in 1 patient with an anterior localization and in 8 patients with an inferoposterior localization. The decrease was sudden in 4 (44.4%), and gradual in 5 (55.6%) of the patients. In 3 patients (33.3%) junction rhythm was developed, and in 2 patients (22.2%) AV block II-III. Only in 2 of them, there was a worsening of regional function during a high dose dobutamine infusion, but 7 of them showed an improvement during a low dose. In 7 (77.8%) of the patients there was a simultaneous decrease in blood pressure. Coronary angiographic examination showed that in 4 (44.4%) of the patients there was a significant coronary artery disease and they underwent the revascularization procedure. During the follow up period, there was not any significant arrhythmic disorder in that group of the patients or repeated hospitalization because of postinfarction angina, re-infarction, or heart failure. Conclusion. We could conclude that paradoxical sinus deceleration is not only an indicator of a significant coronary artery disease and ?bad left ventricle?. It also may occur as a consequence of vasodepressor reflex (Bezold-Jarisch), even after acute myocardial infarction, without influencing a long-term prognosis.


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