Myocardial exchanges of glutamate, alanine and citrate in controls and patients with coronary artery disease

1. Myocardial exchanges of plasma alanine, glutamate, citrate, lactate, glucose and free fatty acids were determined in 17 patients with coronary artery disease and in seven control subjects during rest, atrial pacing and recovery. 2. Myocardial release of alanine was demonstrated in all subjects. The amount released was higher in patients with coronary artery disease than in controls. In the patients alanine release was related to severity of coronary artery stenosis. 3. All subjects showed myocardial uptake of glutamate, higher in patients than in controls at rest and during recovery. During atrial pacing myocardial glutamate extraction remained unchanged in controls but decreased in patients. 4. Citrate was released by the heart in all controls and patients. During recovery citrate output was higher in patients than in controls. 5. Myocardial alanine and citrate release during recovery were positively correlated. Both were positively related to myocardial uptake of glutamate during recovery and to the decrease in glutamate extraction during pacing. 6. The results indicate changed myocardial citrate and amino acid metabolism in coronary artery disease. Measurement of myocardial exchanges of glutamate, alanine and citrate in addition to lactate is suggested as a sensitive biochemical test in assessing myocardial ischaemia in man.     

Alpha adrenoceptor regulation of coronary artery blood flow in normal and stenotic canine coronary arteries

The response of systemic blood pressure, heart rate, lead II ECG and left circumflex (LCX) coronary artery blood flow to left cardiac sympathetic nerve stimulation was measured in pentobarbital-anesthetized, open chest, spinal transected and vagotomized dogs. After beta adrenoceptor blockade, left cardiac sympathetic nerve stimulation produced frequency dependent decreases in LCX blood flow. Selective alpha-2 adrenoceptor blockade with idazoxan produced a greater inhibition of this decrease in LCX blood flow than did selective alpha-1 adrenoceptor blockade with prazosin. In an additional population of dogs which were similarly prepared but were not spinally transectioned or pretreated with a beta adrenoceptor antagonist, left cardiac sympathetic nerve stimulation produced an increase in LCX blood flow in all animals which reached a maximum within 40 sec, and then began to decline slowly. However, after beta adrenoceptor blockade, identical stimulation parameters produced only a decline in LCX blood flow which returned to the level of control resting blood flow by the end of the stimulation period. Both selective alpha-2 adrenoceptor blockade with idazoxan and selective alpha-1 adrenoceptor blockade with prazosin produced an inhibition of the LCX blood flow decrease provoked by left cardiac sympathetic nerve stimulation in dogs pretreated with beta adrenoceptor antagonists. Idazoxan produced a slightly greater inhibition of the LCX blood flow decrease than did prazosin, suggesting a greater role for postjunctional vascular alpha-2 adrenoceptors in LCX blood flow regulation during cardiac sympathetic nerve stimulation. The presence of a severe coronary artery stenosis reduced, but did not inhibit, the increase in LCX blood flow in response to cardiac sympathetic nerve stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial infarction in a patient with normal coronary arteries and hereditary haemorrhagic telangiectasia

Sir, We read with interest the excellent paper by Gallitelli et al.on emergencies in hereditary haemorrhagic telangiectasia (HHT).¹HHT (or Osler-Weber-Rendu disease) is an uncommon autosomaldominant vascular disorder, related to an endoglin or activin-receptor-likekinase 1 (ALK1) gene mutation, resulting in multiorgan vasculardysplasia.² HHT can lead to several     

Myocardial ischemia in severe aortic regurgitation despite angiographically normal coronary arteries

Patients with severe aortic regurgitation frequently present with angina pectoris. The exact pathophysiology for angina in aortic regurgitation is not clear. Left ventricular hypertrophy and myocardial blood supply-demand mismatch have been the suggested mechanisms to explain ischemia. However, no conclusive clinical study exists to define the incidence of ischemia in patients with severe aortic regurgitation and normal coronary arteries. We, therefore, investigated the frequency of myocardial ischemia in relation to left ventricular hypertrophy or dilatation in patients with severe aortic regurgitation and normal coronary arteries. We reviewed the medical records of all patients (n = 311) with aortic valve replacement due to aortic regurgitation between 2007 and 2010. We selected subjects with normal coronary arteries (n =182) for the study purpose, and we identified 35 patients who underwent myocardial perfusion scintigraphy prior to the coronary angiography (19 female and 16 male subjects; age 45.0 ± 8.9 years). Left ventricular hypertrophy and dilatation were detected in 9 (26%) and 5 (14%) patients, respectively. Myocardial perfusion scintigraphy showed evidence of ischemia in 10 (29%) patients with normal coronary arteries. The presence of ischemia did not relate to the presence of left ventricular hypertrophy and/or dilatation. As a potential mechanism, aortic regurgitation causes backflow of blood from the aorta into the left ventricle, hence disturbs coronary flow dynamics. In conclusion, myocardial ischemia is common (nearly one-third) among patients with severe aortic regurgitation even in the absence of coronary obstruction, left ventricular hypertrophy and/or dilatation.     

Myocardial infarction complicating hormone replacement therapy in a young woman with normal coronary arteries

We describe a 30-year-old Afro-Caribbean woman with a history of secondary amenorrhoea, who had been treated with HRT because of a presumed diagnosis of premature ovarian failure, and subsequently presented with an acute infero-lateral myocardial infarction. Subsequent coronary angiography demonstrated normal coronary arteries.     

Validating studies for panic disorder in patients with angiographically normal coronary arteries

This article describes validating studies for diagnosing panic disorder in some patients with angiographically normal coronary arteries (NCA) and chest pain. Psychiatric interviews of 94 such patients showed that 34% met the diagnostic criteria for panic disorder. Further studies showed that NCA patients with panic disorder were more disabled at 3.5-year follow-up, had more relatives with panic disorder, were more likely to suffer from major depression, and were more likely to respond to 35% CO2 challenge with panic symptoms. Because panic disorder is highly disabling but responds well to psychological and pharmacologic treatments, screening NCA patients in the cardiology population for this disorder is recommended.     

Characteristic of fatty acid metabolism in patients with CHD with affected and unaffected coronary arteries

Cardiac syndrome X (CSX) is coronary heart disease (CHD) in the absence of or with minimal atherosclerotic changes in coronary arteries. This condition has a more favourable prognosis than classical angina but is associated with relatively poor quality of life. None of the many hypothesis of angina pathogenesis in CSX patients explains it exhaustively. We undertook to consider minor atherosclerotic changes in patients with CSX based on modem concepts of atherogenesis implying its relation to the level and metabolism of lipid fatty acids. Comparative analysis of their composition in blood and saliva provided material for the characteristic of CHD patients with intact and affected coronary arteries.     

Impaired coronary endothelium-dependent vasodilation is associated with microalbuminuria in patients with type 2 diabetes and angiographically normal coronary arteries

OBJECTIVE: Microalbuminuria and impaired endothelium-dependent vasodilation are both predictors for cardiac events in patients with type 2 diabetes. The aim of the study was to evaluate whether microalbuminuria correlated with coronary endothelium-dependent vasodilation. RESEARCH DESIGN AND METHODS: We evaluated 84 patients (47 men, mean age 50.5 +/- 5.9 years) with type 2 diabetes for 9.4 +/- 3.4 years, without angiographic coronary stenosis and without major cardiovascular risk factors or other confounding factors, for endothelium investigation. Quantitative coronary angiography was used to assess coronary artery response to cold pressor testing, used to assess endothelium-dependent vasodilation, and to isosorbide dinitrate (endothelium-independent vasodilation). RESULTS: Endothelium-dependent vasodilation differed in the patients with and without microalbuminuria (changes in coronary artery diameter during cold pressor testing: -15.0 +/- 1.9% vs. -10.2 +/- 1.3%, respectively, P < 0.05) and correlated with urinary albumin excretion rate (r = -0.39, P = 0.003), diastolic blood pressure (r = 0.29, P < 0.01), and left ventricular mass index (r = -0.24, P < 0.05). Independent predictors for endothelium-dependent vasodilation were urinary albumin excretion rate (beta -0.04 [95% CI -0.07 to -0.01], P < 0.005) and left ventricular mass index (-0.26 [-0.49 to -0.05], P < 0.05). Endothelium-independent vasodilation was similar in both groups. CONCLUSIONS: Type 2 diabetic patients with microalbuminuria have a more severely impaired coronary endothelium-dependent vasodilation than those with normoalbuminuria. These data suggest a common pathophysiological process for both coronary vasomotor abnormalities and microalbuminuria.     

Cardiac arrest in a patient with normal coronary arteries

We describe the case of a 47-year-old woman who presented with the clinical picture typical for the entity described as transient left ventricular apical ballooning syndrome (Takotsubo cardiomyopathy). She presented with chest pain secondary to vasospasm after an emotional argument. Her coronary anatomy was free of significant atherosclerotic lesions, and her ventriculogram revealed apical ballooning in the shape similar to the round-bottomed Japanese pot used for trapping octopus.     

冠状动脉造影正常伴心前区疼痛患者冠状动脉微血管功能的无创性超声多普勒评估

目的　经胸多普勒超声心动图 (TTDE)与冠状动脉内多普勒 (ICD)相对照 ,分析TTDE探测冠状动脉造影正常者左前降支 (LAD)远端血流的准确性 ;分析冠状动脉造影正常者冠状动脉微血管功能的变化。方法　利用TTDE探测 3 5例冠状动脉造影正常者LAD远端的基础状态及经静脉注入腺苷后的最大血流速度 ,计算冠状动脉血流速度储备 (CFVR)、冠状动脉阻力 (CVR )和最小冠状动脉阻力指数 (CVRI)。分析比较 2 0例心前区疼痛患者 (A组 )和 15例正常人 (B组 )上述冠状动脉血流参数测值。结果　 3 5例冠状动脉造影正常者TTDE所探测的基础状态血流速度 (APVb)、最大充血反应状态血流速度 (APVh)和CFVR与ICD的探测结果密切相关 (r分别为 0 .79,0 .83 ,0 .85 )。A组与B组APVb、APVh和CVR的差异均无显著性意义 (P >0 .0 5 ) ,但A组CFVR低于B组 ,而CVRI高于B组 (均P <0 .0 5 )。结论　TTDE是一项可行、可信的无创性探测CFVR的方法。冠状动脉造影正常伴心前区疼痛患者存在冠状动脉微循环功能障碍。     

心肌造影检测冠状动脉微循环内皮损伤的初步应用研究

目的：探讨心肌超声造影（Myocardial contrast echocardiography, MCE）在检测冠心病早期冠脉微循环内皮损伤中的应用价值。资料与方法：选择冠状动脉造影（Coronary angiography, CAG）检查结果正常的患者20例为冠心病高危人群组（第2组）,另选年龄匹配的健康志愿者20例作对照组（第1组）行“声诺维”心肌造影。造影后进行4次闪烁成像,分析两组闪烁显像后心肌血流再灌注充盈曲线,获得再充盈峰值强度（PI）、达峰值强度时间（TP）以及心肌内微泡持续显影时间（T）并作定量分析。结果：第2组4次flash后的峰值强度均低于对照组（P<0.05）,达峰值强度时间（TP）以及心肌内微泡持续显影时间均明显大于对照组（P<0.05）。结论：MCE通过定量评价心肌微循环灌注可达到检测冠状动脉微循环内皮功能损伤的目的。