OBJECTIVEPatient with myocardial bridging (MB) usually has a benign prognosis, but some MB patients might experience myocardial ischemia, infarction and sudden cardiac death, especially during active physical activities. The purpose of the study was to study the stress-induced blood flow changes of the mural coronary artery in MB patients determined by intracoronary Doppler.

METHODSIn 8 patients with MB, the basic average peak velocity (bAPV), hyperemic average peak velocity (hAPV) of blood flow, coronary flow reverse (CFR) proximal and distal to the mural coronary artery were measured before and during intravenously dobutamine (10 microg kg-1 min-1, then add 10 microg kg-1 min-1 at 3 min interval till 40 microg kg-1 min-1) by intracoronary Doppler.

RESULTSThe baseline mural coronary diameter reduction was (51.7+/-21.4)% and significantly increased to (90.0+/-12.7)% (P<0.01) during dobutamine infusion. bAPV on the segments proximal and distal to the mural coronary artery significantly increased from (19.83+/-5.84) cm/s and (20.75+/-4.91) cm/s to (31.52+/-10.93) cm/s and (30.46+/-9.01) cm/s (all P<0.05 vs. baseline) respectively post dobutamine infusion. CFR measured at proximal and distal to myocardial bridging also significantly decreased from (2.91+/-0.62) and (2.46+/-0.82) to (2.17+/-0.66) and (1.83+/-0.51) (all P<0.01).

CONCLUSIONStress can significantly increase the compression of intramural coronary artery and reduce CFR on coronary segments both proximal and distal to the MB. Thus, active exercise might induce myocardial ischemia in patients with myocardial bridging.

Blood Flow Velocity ; Cardiotonic Agents ; pharmacology ; Coronary Circulation ; drug effects ; Coronary Vessel Anomalies ; physiopathology ; Coronary Vessels ; drug effects ; Dobutamine ; pharmacology ; Female ; Humans ; Male ; Middle Aged

It has been reported that a change in the cellular redox state may be involved in the regulation of vascular tone, but the underlying mechanism is not fully understood. The present study was designed to investigate the cellular effect of sulfhydryl modifying agents in the coronary artery of rabbit using the tension measurement and whole cell clamping method. The application of diamide, a sulfhydryl oxidizing agent, relaxed the endothelium denuded coronary arteries in a dose dependent manner. The fact that this diamide-induced relaxation was significantly attenuated by a pretreatment of 4-AP, and the coronary arteries precontracted with 100 mM K+ instead of histamine, suggests the involvement of 4-AP sensitive K+ channels in the diamide-induced relaxation of coronary arteries. Whole cell patch clamp studies revealed that the 4-AP sensitive IdK was significantly enhanced by the membrane permeant oxidizing agents, diamide and DTDP, and were reversed by subsequent exposure to the reducing agent, DTT. Neither the membrane impermeant oxidizing or reducing agents, GSSG or GSH, had any effect on the activity of IdK, indicating that intracellular sulfhydryl modification is critical for modulating IdK activity. The Diamide failed to significantly alter the voltage dependence of the activation and inactivation parameters, and did not change the inactivation process, suggesting that diamide increases the number of functional channels without altering their gating properties. Since IdK has been believed to play an important role in regulating membrane potential and arterial tone, our results about the effect of sulfhydryl modifying agents on coronary arterial tone and IdK activity should help understand the pathophysiology of the diseases, where oxidative damage has been implicated.
Animal ; Arteries/physiology ; Arteries/drug effects ; Arteries/cytology ; Coronary Vessels/physiology ; Coronary Vessels/drug effects* ; Coronary Vessels/cytology ; Female ; Male ; Oxidants/pharmacology* ; Potassium Channels/physiology ; Rabbits ; Reducing Agents/pharmacology* ; Sulfhydryl Compounds/metabolism*

BACKGROUNDCoronary endothelial shear stress (ESS) triggered the development of atherosclerosis. However, the effect of calcium channel antagonist on the distribution of ESS remained unclear.

METHODSTwenty consecutive patients with acute coronary syndrome (ACS) 48 hours after maximal medication with single left anterior descending artery stenosis < 50% were studied. Nicardipine was intravenously injected at 1 µg/kg after a bolus of 10 mg in order to achieve mean blood pressure (MBP) reduced by 10% or more, or the heart rate increased by 10 - 15 beats/min. Hemodynamic variables and angiogram at baseline and during injection of nicardipine were recorded, respectively. Coronary artery 3-D reconstruction was used for the analysis of ESS.

RESULTSDistal reference-vessel-diameter and minimal lumen diameter decreased significantly from (2.42 ± 0.41) mm and (1.47 ± 0.49) mm at baseline to (2.22 ± 0.35) mm and (1.35 ± 0.49) mm at maximal drug-dosage (P = 0.018 and 0.020, respectively). Nicardipine did not change blood velocity. Lowest mean shear stress at segments 2-mm distal to plaque increased significantly from (0.034 ± 0.519) Pa at baseline to (0.603 ± 0.728) Pa (P = 0.013) at peak effect of drug.

CONCLUSIONSNicardipine was associated with the constriction of diseased vessel segment that adapted to the reduction of blood pressure, without dynamic change of blood velocity at each stage of whole cardiac cycle. Increased ESS value at segments distal to plaque reflected the cardioprotection by nicardipine (ChiCTR-TRC-10000964).

Acute Coronary Syndrome ; Aged ; Angina, Unstable ; diagnostic imaging ; drug therapy ; Blood Pressure ; drug effects ; Coronary Angiography ; Coronary Vessels ; drug effects ; Female ; Heart Rate ; drug effects ; Hemodynamics ; drug effects ; Humans ; Male ; Middle Aged ; Nicardipine ; therapeutic use

Aged ; Angioplasty, Balloon, Coronary ; adverse effects ; Coronary Vessels ; injuries ; Drug-Eluting Stents ; Humans ; Male ; Polytetrafluoroethylene ; chemistry ; therapeutic use

No abstract available.
*Angioplasty, Balloon, Coronary ; Coronary Artery Disease/*drug therapy ; Coronary Vessels/*drug effects/pathology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology ; Metals ; Simvastatin/*pharmacology ; *Stents ; Ultrasonography, Interventional

This study was designed to clarify the dependency of hypoxic coronary vasodilation (HCD) on the endothelium and the role of the K+ channels on HCD in the rabbit coronary artery. HCD was investigated in an isolated left circumflex coronary artery precontracted with prostaglandin F2 alpha. Vascular rings were suspended for isometric tension recording in an organ chamber filled with Krebs-Henseleit (KH) solution. Hypoxia was induced by gassing the chamber with 95% N2 + 5% CO2 and was maintained for 15 approximately 25 min. Hypoxia elicited a vasodilation in the precontracted coronary artery with and without endothelium. There was no difference between the amplitude of the HCD induced by two consecutive hypoxic challenges and the effects of 20% O2 + 5% CO2 + 75% N2 and 95% O2 + 5% CO2 control K-H solution of subsequent responses to hypoxia. Inhibition of the cyclooxygenase pathway by treatment with indomethacin had no effect on HCD. Blockades of the tetraethylammonium chloride-sensitive K+ channel abolished HCD. Apamin, a blocker of the small conductance Ca(2+)-activated K+ (KCa) channel, and iberiotoxin, a blocker of the large conductance KCa channel had no effect on HCD, respectively. Glibenclamide, a blocker of the ATP-sensitive K+ (K+ATP) channel, reduced HCD. Cromakalim, an opener of the K+ATP channel, relaxed the coronary artery precontracted with prostaglandin F2 alpha. The degree of relaxation by cromakalim was similar to that by hypoxia while glibenclamide reduced both hypoxia- and cromakalim-induced vasodilatations. In conclusion, these results suggest that HCD is independent on endothelium and HCD is considered to be induced by activation of K+ATP channel.
Animal ; Anoxia/physiopathology* ; Coronary Vessels/physiopathology* ; Coronary Vessels/drug effects ; Cyclooxygenase Inhibitors/pharmacology ; Enzyme Inhibitors/pharmacology ; Female ; Indomethacin/pharmacology ; Male ; Nitroarginine/pharmacology ; Rabbits ; Tetraethylammonium/pharmacology ; Vasodilation/physiology*

OBJECTIVETo evaluate the effect of Shexiang Baoxin Pill (SBP) on coronary vasodilation by analysis of coronary angiography (CAG).

METHODSA consecutive cohort of 300 patients who underwent CAG between January 2013 and July 2013 were recruited and randomly assigned to 2 groups before operation. Patients in the SBP group sublingually took SBP, while those in the control group sublingually took placebos. All patients repeatedly underwent CAG 5 min after administration. The vascular diameter was calculated by quantitative angiography analysis method. The diameter of the left anterior descending coronary artery was measured in patients whose coronary arteries had no stenosis. The narrowest vascular diameter was measured in patients whose coronary arteries had stenosis. The heart rate, blood pressure, and the vascular diameter were compared between before and after administration in the two groups.

RESULTSIn the two groups, there was no significant difference in changes of heart rate, systolic pressure, or diastolic pressure between before and after administration (all P > 0.05). There were 64 patients with normal CAG in the two groups, 30 in the control group and 34 in the SBP group. CAG showed there were 236 patients with stenotic coronary artery, 110 in the control group and 126 in the SBP group. The vascular diameter was obviously larger in patients in the SBP group with normal or abnormal CAG after administration (all P < 0.01). It was also obviously larger than that of the control group after administration (P < 0.05, P < 0.01).

CONCLUSIONSBP could dilate both normal coronary artery and lesioned coronary arteries, but did not lead to fastened heart rate and decreased blood pressure.

Blood Pressure ; Coronary Angiography ; Coronary Vessels ; drug effects ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; therapeutic use ; Heart Rate ; Humans ; Tablets ; Vasodilation ; drug effects

Cardiovascular diseases, like coronary heart disease and myocardial infarction, are the most common cause of death worldwide. Chinese medicines have demonstrated rich cardioprotective activities for clinical applications. Salvia miltiorrhiza, a very important component of traditional Chinese medicine, can promote blood circulation and relieve blood stasis. Salvia miltiorrhiza is widely used in treatment of cardiovascular and cerebrovascular disease such as coronary heart disease and cerebral infarction ( CI). Tanshinone II(A), the major lipophilic components extracted from the root of S. miltiorrhiza, possesses anti-atherosclerosis, anti-cardiac hypertrophy, anti-oxidant, anti-arrhythmia and so on. This paper discusses current research status of tanshinone II(A) in cardioprotective effects.
Animals ; Cardiovascular Diseases ; drug therapy ; genetics ; metabolism ; physiopathology ; Coronary Vessels ; drug effects ; physiopathology ; Diterpenes, Abietane ; therapeutic use ; Humans

OBJECTIVETo evaluate the direct effects of dobutamine as compared to adenosine on the coronary microcirculation in both normal and stenotic segments using myocardial contrast echocardiography (MCE).

METHODSLeft anterior descending (LAD) coronary artery stenosis, which was not flow limiting at rest, was established in 9 dogs. At the baseline and during intracoronary infusion of dobutamine (2 mg.kg(-1).min(-1)) and adenosine (5 mg.kg(-1).min(-1)), the radiolabeled microsphere (RM)-derived myocardial blood flow (MBF) were determined, and the double product (DP) and myocardial vascular resistance (MVR) were calculated. MCE was performed to determine the myocardial blood volume (MBV, represented by A) and microbubble velocity (beta).

RESULTSAs compared to the baseline level, the MBF increased and MVR decreased significantly in both the normal and abnormal beds during infusion of both drugs (P<0.05). In the normal bed, adenosine had no effect on MBV, the decrease in MVR was the result of decreased arteriolar (plus venular) resistance, and the increase in MBF was predominately due to the increase in b (deltabeta/ deltaA=13.6). Dobutamine caused a 28% increase in MBV, responsible for 32% of the decrease in the total MVR, but the increase in MBF arose mainly from the increase in b (deltabeta/deltaA=5.9). In the abnormal bed, both the drugs caused a similar increase in MBF entirely by increasing b, and 14% and 15% of the increases in capillary resistance were associated with the capillary derecruitment during administration of dobutamine and adenosine, respectively.

CONCLUSIONThe direct effects of intracoronary dobutamine infusion on the coronary microcirculation are similar to that of adenosine, and the increase in MBF occurs mostly as the result of increased myocardial blood velocity.

Adenosine ; pharmacology ; Adrenergic beta-Agonists ; pharmacology ; Animals ; Blood Flow Velocity ; drug effects ; Coronary Circulation ; drug effects ; Coronary Stenosis ; diagnostic imaging ; Coronary Vessels ; diagnostic imaging ; Dobutamine ; pharmacology ; Dogs ; Echocardiography ; methods ; Microcirculation ; drug effects ; Vasodilator Agents ; pharmacology

Native coronary artery spasm after coronary artery bypass grafting (CABG) is scarce. It frequently causes disastrous circulatory collapse. We report a 72-yr-old male, who experienced native coronary artery spasm and grafted artery spasm following CABG, which was successfully treated with coronary angiography and intracoronary injection of nitroglycerine.
Aged ; Coronary Angiography ; Coronary Artery Bypass/*adverse effects ; Coronary Vasospasm/drug therapy/*etiology ; *Coronary Vessels/drug effects/physiopathology/surgery ; Humans ; Male ; Nitroglycerin/therapeutic use ; Treatment Outcome ; Vasodilator Agents/therapeutic use