No abstract available.
Anesthesia, Spinal* ; Coronary Vasospasm* ; Epinephrine*

No abstract available.
Anesthesia, Spinal* ; Coronary Vasospasm* ; Epinephrine*

No abstract available.
Coronary Vasospasm* ; Heart Arrest* ; Verapamil*

No abstract available.
Coronary Vasospasm* ; Death, Sudden, Cardiac* ; Smoke* ; Smoking*

Intercoronary arterial connection between normal coronary arteries is a rare variant of coronary anatomy in which there is open-ended circulation. It is distinguished from collaterals seen in the occlusive coronary artery disease. We report a case of bidirectional intercoronary communication between the left circumflex artery and the right coronary artery without occlusive coronary artery disease, but with left anterior descending artery spasm.
Arteries ; Coronary Artery Disease ; Coronary Vasospasm ; Coronary Vessel Anomalies ; Coronary Vessels ; Spasm

Coronary Vasospasm ; diagnosis ; Female ; Humans ; Myocardial Ischemia ; diagnosis

OBJECTIVEThis coronary artery spasm review aimed to explore the most possible pathogenic trigger mechanism of vulnerable plaque rupture.

DATA SOURCESData used in this coronary artery spasm review were mainly from Medline and Pubmed in English.

STUDY SELECTIONThese reports from major review on coronary artery spasm. and these research included coronary artery conception, pathogenesis of spasm, mechanisms of plaque rupture, epidemiological evidence, clinical manifestation and the relationship between coronary artery spasm and vulnerable plaque rupture.

RESULTSCoronary artery spasm is somehow related to the presence of atherosclerotic intima disease in the coronary artery. However, chronic low-grade inflammation causes coronary vessel smooth muscle cell hypersensitivity, which can directely cause coronary artery spasm. Myocardial infarction and sudden cardiac death may be initiated by a sudden intense localized contraction of coronary artery smooth muscle.

CONCLUSIONCoronary artery spasm may be one trigger that can initiate and exacerbate vulnerable plaque rupture.

Diagnosing and selecting an appropriate treatment strategy for left main coronary artery (LMCA) obstruction is very important. Although this disease is not frequently encountered, it can cause severe hemodynamic deterioration resulting in a less favorable prognosis without a suitable management approach. Another aspect of LMCA that we must not overlook is coronary artery spasm, which can be an infrequent but important cause of acute coronary syndrome. Although it is rare, LMCA can cause critical complications. In this study, we report the case of a 35-year-old female who was admitted to the hospital with a diagnosis of acute myocardial infarction with ST-segment elevation in the aVR lead caused by a left main coronary spasm that was examined on intravascular ultrasound.
Acute Coronary Syndrome ; Adult ; Coronary Vasospasm ; Coronary Vessels ; Electrocardiography ; Female ; Hemodynamics ; Humans ; Myocardial Infarction ; Prognosis ; Spasm

OBJECTIVETo observe the feasibility of establishing a porcine model of microvascular coronary artery spasm by intracoronary neuropeptide Y (NPY) infusion, and to analyze the characterization of this model.

METHODSMinipigs were divided into four groups (n = 4 each): normal saline (NS) group, 1 nmol NPY group, 3 nmol NPY group, and 6 nmol NPY group. Arterial sheaths were planted into bilateral femoral arteries of minipigs. A pigtail catheter was placed at the left sheath to determine the hemodynamic parameters. NS and different doses of NPY were injected into the left anterior descending branch through the right sheath. Intravenous myocardial contrast echocardiography (MCE) was applied to measure the microvessel volume (α), filling velocity (β), and microcirculation blood flow (MBF) before and at 10 and 30 minutes after NS and NPY injection.

RESULTSBefore and after injection, there were no difference in α, β and MBF between NS and 1 nmol NPY group (all P > 0.05). In 3 nmol NPY group, α and MBF decreased at 10 min (P < 0.01 and 0.05, respectively), which were recovered at 30 min except α. Reductions of β (P < 0.05) and MBF (P < 0.01) were observed at 10 min in 6 nmol NPY group, which were recovered at 30 min, but MBF still remained lower than at baseline (P < 0.01) and compared to 3 nmol NPY group (P < 0.05).

CONCLUSIONIntracoronary injection of NPY into the anterior descending coronary artery can establish the porcine model of microvascular coronary artery spasm, which might serve as a useful animal model for coronary microvascular studies.

Isometric tension recording was performed in the transverse strips of porcine coronary arteries and rabbit aorta to observe the effects of the endothelium and endothelium-derived relaxing factor(EDRF) on vasomotor tone and to test the hypothesis that alcohol may have the deleterious effect on endothelium-dependent vasorelaxation. Tension-development by vasoconstrictor was markedly attenuated in the endothelium-intact strips compared to the endothelium denuded strips. Administration of hemoglobin(10-5M) to inhibit the action of EDRF increased tension selectively in the endothelium-infarct strips, which is suggestive of basal EDRF secretion. Nitro L-arginine(10-5M). an analogue of L-arginine(10-4M) partially reversed the inhibitory effect of nitro L-arginine. Ethyl alchol inhibited bradykinin-induced endothelium-dependent vasorelaxation of porcine coronary artery in dose dependent manner. These data suggest that the protective effect of vascular endothelium to the action of vasoconstirctor can be explained by exercise of basal EDRF release and damaged endothelium would be a great risk of induction of vasospasm. Also we believe that there is a relationship of competive inhibition between L-arginine. a precursor of EDRF, and its analogues on the action of EDRF and alcohol intake would be hazardous to the patients with coronary artey disease because its inhibitory action on endothelium-dependent vasorelaxation may evoke myocardial ischemia.
Aorta ; Arginine ; Coronary Vasospasm ; Coronary Vessels* ; Endothelium* ; Endothelium, Vascular ; Ethanol* ; Humans ; Myocardial Ischemia ; Spasm* ; Vasodilation