Silent Angina Research Articles

Characteristics of the severity of the early formation of the atherosclerotic process in certain pathological forms of coronary heart disease in marine specialists in the conditions of the Arctic region

The present work aims to study lipid balance, specifi markers of atherosclerosis, morphological changes in the main arteries, as well as paired indicators, in the formation of the atherosclerotic process in some non-comorbid pathological forms (painful/silent episodes of angina pectoris) of chronic coronary artery disease occurring with affective disorders in shipboard personnel serving in the Far North. The study revealed a higher incidence of structural changes in the medial sheath of both common carotid arteries in silent angina pectoris, which are manifested in vascular bed remodeling, formation of atherosclerotic plaques, and stenotic atherosclerosis. In addition, an increase in proatherogenic activity, suppression of antiatherogenic parameters, as well as more significant changes in the paired indicators of the atherosclerotic process were observed in such patients. The exacerbation of the main pathological process in chronic coronary artery disease can be attributed to the existing polymorbidity.

Serotonin-Mediated Cardiac Analgesia via Ah-Type Baroreceptor Activation Contributes to Silent Angina and Asymptomatic Infarction

Silent angina is a critical phenomenon in the clinic and is more commonly associated with women patients suffering from myocardial ischemia. Its underlying cause remains mysterious in medicine. With our recent discovery of female-specific Ah-type baroreceptor neurons (BRNs), we hypothesize that cardiac analgesia is due to the direct activation of Ah-type BRNs by elevated levels of circulating serotonin (5-HT) myocardial infarction (MI) patients. Electromyography and the tail-flick reflex were assessed in control and MI-model rats to evaluate 5-HT-mediated BP regulation as well as peripheral and cardiac nociception. 5-HT or a 5-HT receptor agonist was microinjected into the nodose ganglion to confirm the involvement of the afferent pathway of the baroreflex arc. An inward current was observed in identified BRNs by applying a whole-cell patch-clamp technique in conjunction with qRT-PCR to verify the afferent-specific action of 5-HT and the expression of 5-HT receptors. Although the tail-flick reflex and mean arterial pressure were dramatically reduced in female MI rats with elevated serum 5-HT, intrapericardial capsaicin-evoked muscular discharges were significantly inhibited in comparing with those of males, which were mimicked by microinjection of 5-HT or SR57227A into the nodose. Ah-type BRNs displayed robust inward currents at lower concentrations of 5-HT than the C-type or the A-type, with significantly increased expression and cellular distribution of 5-HT3AR but not 5-HT3BR compared to the A- and C-types. Activation of 5-HT3AR in Ah-type BRNs by 5-HT contributes significantly to cardiac analgesia, which may suggest the pathogenic condition that silent angina occurs mainly in female patients.

Bioresorbable everolimus-eluting vascular scaffold for patients presenting with non STelevation-acute coronary syndrome: A three-years follow-up1

To investigate three-year outcomes of patients presenting with nonSTelevation acute coronary syndrome (NSTE-ACS) treated with bioresorbable everolimus-eluting vascular scaffolds (BRS). The study included a total of 488 consecutive patients, enrolled between May 2012 and December 2013 (median age 65 [56-74], 392 men. 269 patients presented with either NSTEMI or unstable angina at the time of enrolling, 219 patients with stable or silent angina. The primary device-oriented endpoint (Target Lesion Failure, TLF) was defined as a combination of cardiovascular death, target vessel myocardial infarction or clinically driven target lesion revascularization.Among the cardiac risk factors, NSTE-ACS patients were more frequently smokers (P = 0.028), had less frequently dyslipidemia (P = 0.003) and a history of prior PCI (P < 0.01).The median follow-up was 1070[763-1197] days. The three-years incidence of TLF was slightly higher but did not differ significantly between groups (NSTE-ACS: 16.3% vs. 15.9%, p = 0.163). Accordingly, there was no difference in any of the other endpoints. Treatment of NSTE-ACS with BRS appears to be safe and effective. In this group, risk factors for events during follow up did not differ as compared to the general population.

The variable morphological coexistence of apoptosis and necrosis in human myocardial infarction: significance for understanding its pathogenesis, clinical course, diagnosis and prognosis.

Myocardial infarction includes both apoptosis and necrosis, but little is known of the morphological relationship of these two different forms of cell death in the human heart, despite the possibility that this may have clinical importance. Hearts from 77 cases of fatal myocardial infarction were examined. Twelve morphologically representative hearts were selected for immunohistochemical staining to define in detail the histology and cytology of apoptotic areas. Both apoptosis and necrosis were present in every heart. Necrotic myocytes quickly disintegrate and evoke acute inflammation. Apoptotic myocytes retain their membrane integrity and do not evoke acute inflammation. Phagocytosis of apoptotic cells and apoptotic bodies occurred with engulfment by either neighboring myocytes or macrophages, but predominantly the latter. In many apoptotic areas, the phagocytic capacity was overwhelmed, resulting in large pools of apoptotic bodies lying free in the extracellular space. Because apoptotic cells retain their membrane integrity, enzymatic diagnosis of myocardial infarction that is due to necrosis. Measurement of any intracellular enzyme consequently always underestimates the extent of myocardial infarction, often by a large margin. Morphological progression of cell death in myocardial infarction, from apoptosis to necrosis, may depend upon exceeding the local capacity for phagocytosis of apoptotic cells. However, cells dying by either apoptosis or necrosis are equally dead. There is a need for better definition of the role of apoptosis in myocardial hibernation (or stunning), in ischemic preconditioning and in the pathogenesis of silent angina, and post-myocardial infarction remodeling.

Dipyridamole-echocardiography test in essential hypertensives with chest pain and angiographically normal coronary arteries.

Microvascular angina--chest pain syndrome in the presence of angiographically normal epicardial coronary arteries and reduced flow reserve--has been described in patients with essential hypertension (EH) and linked to the development of left ventricular hypertrophy (LVH). We performed a dipyridamole-echocardiography test (DET: 2D-echo and 12 lead ECG monitoring with dipyridamole infusion, up to 0.84 mg/kg over ten minutes) in 28 essential hypertensives meeting the following inclusion criteria: (1) history of chest pain; (2) angiographically normal coronary arteries; (3) normal resting regional and global left ventricular function. A group of 12 (age- and sex-matched) normotensives with the same inclusion criteria, as well as with negative exercise stress test, was also evaluated. During DET, none of the essential hypertensives or the control group developed a regional dyssynergy of contraction. Fifteen essential hypertensives and two in the control group had a diagnostic (greater than 0.1 mV from baseline) ST segment depression on ECG tracing (54 v 17%, P less than .01); 16 essential hypertensives and two in the control group had chest pain (57 v 17%, P less than .01). None of the control group and nine of the essential hypertensives had echocardiographically assessed LVH. In the essential hypertensive group ventricular hypertrophy was present in seven of 20 patients with and in two of eight patients without dipyridamole induced chest pain and/or ST segment depression (35% v 25%, P = NS). In conclusion, essential hypertensive patients with chest pain and angiographically normal coronary arteries frequently show echocardiographically silent angina and/or ST segment depression during DET.(ABSTRACT TRUNCATED AT 250 WORDS)

Silent angina and coronary bypass surgery

Silent angina and coronary bypass surgery