Significant Left Coronary Artery Disease Research Articles

Acute Thrombotic Occlusion of Non-Dominant Right Coronary Artery Presenting as Acute Coronary Syndrome and Hemodynamic Instability

It is generally believed that the occlusion of a non-dominant right coronary artery is not associated with significant consequences. Atherosclerotic disease of non-dominant right coronary in the absence of significant left coronary artery disease is rare, and the prevalence is substantially lower as compared to dominant right coronary artery. We report a case of young male presenting with acute coronary syndrome and hemodynamically significant atrial fibrillation. Coronary angiography showed thrombotic occlusion of non dominant right coronary artery. After the stenting of this artery, patient improved hemodynamically with complte resolution of ECG changes.

Successful intracoronary thrombolysis for extensive right coronary artery luminal thrombotic occlusion

A 46-year-old man who had failed primary angioplasty to the dominant right coronary artery due to high thrombus burden 2 years previously, presented with non-ST-elevation myocardial infarction following discontinuing antiplatelet therapy for 2 months. Angiography showed occluded right coronary artery with extensive thrombus burden. There was no significant left coronary artery disease. Due to failure of thromboaspiration and angiojet from the previous attempt 2 years previously, intracoronary thrombolysis with streptokinase was administered via thromboaspiration catheter. Following intracoronary thrombolysis, aspiration catheter was able to retrieve the majority of thrombi and achieved thrombolysis in myocardial infarction 3 flow at the end of the procedure with resolution of transient ST elevation. This case demonstrated that the use of adjunctive intracoronary thrombolysis and manual aspiration in a patient presenting with myocardial infarction with heavy thrombus burden might be useful in selected cases.<Learning objective: The use of adjunctive intracoronary thrombolysis and manual aspiration in a patient presenting with myocardial infarction with heavy thrombus burden might be useful in selected cases.>

Acute myocardial ischaemia induces cardiac carnitine release in man.

In animal studies, prolonged periods of ischaemia decrease the cardiac carnitine content. However, whether in humans the heart loses carnitine during short-term ischaemia, and whether this is related to ischaemia-induced cardiac dysfunction, is as yet unknown. Carnitine kinetics were investigated in 28 normotensive patients with significant left coronary artery disease, during and after incremental atrial pacing. To evaluate carnitine kinetics from the ischaemic area, patients were grouped as those with (n = 22) or without (n = 6) myocardial lactate production. Atrial pacing resulted in a comparable maximal heart rate and ST depression in both groups. Carnitine kinetics did not change in those without lactate production. In contrast, coronary venous free carnitine levels increased significantly by 9% during pacing in those with lactate production. Cardiac free carnitine balance changed from uptake (255 +/- 107 pmol.min-1, mean +/- SEM) to release, (-150 +/- 66 pmol.min-1) at 30 min after pacing in the group with lactate production. Arterial and coronary venous differences in free carnitine were significantly correlated with myocardial lactate extraction immediately after pacing. The change in coronary venous free carnitine was significantly correlated with the change in left ventricular ejection fraction at 10 min after pacing. Thus, in patients with coronary artery disease, short-term mild myocardial ischaemia results in significant cardiac free carnitine loss.

Estimation of coronary flow reserve by transesophageal coronary sinus Doppler measurements in patients with syndrome X and patients with significant left coronary artery disease

This study sought to determine the feasibility of coronary sinus flow velocity analysis by transesophageal Doppler echocardiography for estimation of coronary flow reserve in patients with syndrome X and patients with coronary artery disease. Coronary flow reserve provides useful information in patients with coronary artery disease and patients with syndrome X. Current methods of measuring coronary flow reserve are invasive or require extensive laboratory equipment, or both. Transesophageal Doppler recordings of coronary sinus flow velocity before and after vasodilator application may allow noninvasive determination of coronary flow reserve. We obtained coronary sinus flow velocity recordings before and after dipyridamole administration (0.6 mg/kg body weight per 5 min) in 9 patients with syndrome X, 14 with significant left coronary artery disease and 22 age-matched control patients. We used the formula anterograde minus retrograde flow velocity time integral times heart rate as an index of coronary sinus flow. Coronary flow reserve was calculated by dividing coronary sinus flow variables after dipyridamole administration by the respective baseline values. Technically adequate recordings were obtained in 44 (98%) of 45 patients. Compared with that in the control group (2.78 +/- 0.95 [mean +/- SD]), coronary flow reserve was significantly lower in patients with syndrome X (1.21 +/- 0.23, p < or = 0.001) as well as in those with coronary artery disease (1.47 +/- 0.7, p < or = 0.001). Using a cutoff coronary flow reserve value of 1.8, sensitivity, specificity and overall predictive value of coronary flow reserve determinations were, respectively, 100%, 91% and 94% for syndrome X and 86%, 91% and 89% for coronary artery disease. Coronary flow reserve calculation by transesophageal coronary sinus flow velocity recordings is feasible in a large proportion of patients and might be useful for the noninvasive evaluation of patients with syndrome X and patients with severe left coronary artery disease.

Significance and treatment of nocturnal angina preceding myocardial infarction

The presence of nocturnal angina and congestive heart failure within the month prior to admission was evaluated in the 174 patients with acute myocardial infarction. Heart size was evaluated radiographically at the time of admission. Twenty-three patients (13 per cent) experienced nocturnal angina. The incidence of nocturnal angina was significantly higher in those with anterior myocardial infarction (p less than 0.005) and subendocardial infarction (p less than 0.02) when compared with patients with inferior MI. Congestive heart failure was more common prior to admission in those with nocturnal angina (9/23) as opposed to those without (3/141) (p less than 0.001). Cardiomegaly was seen in 9/23 patients with nocturnal angina and 22/141 without (p less than 0.02). We conclude that the presence of nocturnal angina in those who develop MI increases the likelihood that the infarction will be either anterior or subendocardial rather than inferior. The association of nocturnal angina and congestive heart failure to anterior myocardial infarction is probably due to more severe and probably significant left coronary artery disease.