This study investigated whether trinitroglycerine (TNG) as nitric oxide (NO) releasing agent had anti-leishmanial effects and mediated pathology in BALB/c mice infected with Leishmania major. Cutaneous leishmaniasis (CL), a zoonotic infection caused by leishmania protozoa is still one of the health problems in the world and in Iran. NO is involved in host immune responses against intracellular L. major, and leishmania killing by macrophages is mediated by this substance. Moreover, application of CL treatment with NO-donors has been recently indicated. In our study, TNG was used for its ability to increase NO and to modify CL infection in mice, in order to evaluate NO effects on lesion size and formation, parasite proliferation inside macrophages, amastigote visceralization in target organs, and NO induction in plasma and organ suspensions. Data obtained in this study indicated that TNG increased plasma and liver-NO, reduced lesion sizes, removed amastigotes from lesions, livers, spleens, and lymph nodes, declined proliferation of amastigotes, hepatomegaly, and increased survival rate. However, TNG reduced spleen-NO and had no significant effects on spelenomegaly. The results show that TNG therapy reduced leishmaniasis and pathology in association with raised NO levels. TNG had some antiparasitic activity by reduction of positive smears from lesions, livers, spleens, and lymph nodes, which could emphasize the role of TNG to inhibit visceralization of L. major in target organs.
Leishmania major; BALB/c mouse; nitric oxide; trinitroglycerin; Iran
Background and Objectives
The intracoronary injection of acetylcholine (Ach) has been shown to induce coronary spasms in patients with variant angina. Clinical significance and angiographic characteristics of patients with a significant response to lower Ach dosages are as-yet non-clarified compared with patients responding to higher Ach doses.
Subjects and Methods
A total of 3034 consecutive patients underwent coronary angiography with Ach provocation tests from January 2004 to August 2010. Ach was injected in incremental doses of 20, 50, 100 µg into the left coronary artery. Significant coronary artery spasm was defined as focal or diffuse severe transient luminal narrowing (>70%) with/without chest pain or ST-T change on the electrocardiogram (ECG). We compared the clinical and angiographic characteristics of patients who responded to a lower Ach dose (20 or 50 µg, n=556) to those that responded to a higher Ach dose (100 µg, n=860).
The baseline clinical and procedural characteristics are well balanced between the two groups, except diabetes was higher in the lower Ach dose group and there were differences in medication history. After adjusting for confounding factors, the lower Ach dose group showed more frequent temporary ST elevation and atrioventricular block on the ECG. Furthermore, the group of patients who responded to the lower Ach dose was associated with a higher incidence of baseline and severe spasm than those who responded to a higher Ach dose.
Patients with a significant response to a lower Ach dose were associated with more frequent ST elevation, baseline spasm, and more severe spasm compared with those who responded to a higher Ach dose, suggesting more intensive medical therapy with close clinical follow-up is required for those patients.
Angina pectoris, variant; Acetylcholine
An 80-year-old man was admitted to the emergency department of our institution due to acute, anterior-wall myocardial infarction and cardiogenic shock. Two-dimensional echocardiography revealed systolic anterior motion of the mitral leaflets with severe left ventricular outflow tract obstruction. Although coronary angiography showed normal coronary arteries, an ergonovine provocation test induced diffuse coronary constriction of the left coronary artery, with chest pain, and ST-T changes seen on the electrocardiogram. These clinical signs caused us to suspect coronary spasm.
The present case serves as a reminder that coronary vasospasm may be a factor in the development of dynamic left ventricular outflow tract obstruction. Early detection and intensive efforts to relieve vasospasm, including emergency coronary angiography and intracoronary injection of nitroglycerin, are essential.
Myocardial infarction/therapy; angina pectoris; shock, cardiogenic; coronary vasospasm/complications/diagnosis/therapy; left ventricular outflow tract obstruction/diagnosis/therapy
Spontaneous severe multivessel coronary artery vasospasm is a rare but important cause of morbidity. One-third of patients have normal coronary vasculature, and these pose a significant therapeutic dilemma as lack of clinical suspicion might potentially lead to unnecessary revascularization therapies. A patient with resting chest pain and ischaemic electrocardiography demonstrated severe coronary obstruction at catheter angiography. Preangioplasty further information highlighted spasm as the likely cause and the angiographic abnormalities resolved post intracoronary nitrate. This paper emphasises thorough history-taking and judicious use of nitrates during diagnostic coronary angiography in such patients. This may negate the need for more complex cardiac interventions.
Nitroglycerin (TNG) causes a prolonged dilatation of coronary collaterals. To demonstrate a functional significance of this dilatation we measured the effect of TNG on myocardial contractile force in dogs 2½-4 wk after the left anterior descending coronary artery (LAD) had been embolized in closed-chest animals. Development of collaterals was documented by angiography. Via a left thoracotomy the main left coronary artery (LCA) and LAD distal to the embolized plug were cannulated. Coronary flow and perfusion pressure were recorded. Contractile force was measured with gauges sutured to epicardial areas supplied by the left circumflex coronary artery (LCf) and occluded LAD. Coronary perfusion pressure in the LCA was gradually decreased until the contractile force recorded by the LAD gauge diminished while the LCf gauge was unaffected. Under these conditions, with coronary perfusion pressure held constant with the aid of a Starling resistance, TNG (18 μg) injected into the LCA increased peripheral LAD pressure by 3-12 mm Hg and contractile force in the LAD region by 36% (range 20-90%), returning it to near-normal levels, while having minimal effect in the LCf area. These changes persisted for 5 min. When LCf and LAD areas were both ischemic, intracoronary TNG had minimal effect on peripheral LAD pressure and contractile force. Thus, TNG causes prolonged dilatation of coronary collaterals and presumed increased collateral flow with subsequent enhancement of myocardial contractile force in ischemic areas. This effect is seen only when ischemia is limited to an area supplied by the collaterals. When the whole heart is ischemic, collaterals are unresponsive to TNG, suggesting that these collaterals dilate fully when the regions from which they originate become ischemic.
A 23 year old man presented with a clinical history and ECG compatible with acute myocardial infarction, having taken a single tablet of ecstasy (3,4-methylenedioxymetamphetamine) 18 hours previously. He was treated with aspirin and thrombolytic therapy; however, cardiac catheterisation showed angiographically normal coronary arteries and left ventricular function. Sympathomimetic drugs are freely available and widely abused in Britain, but there is little evidence of the mechanisms or management of cardiac complications. In such cases the use of standard treatment for acute myocardial infarction is recommended with agents such as glyceryl trinitrate and phentolamine to reduce coronary artery spasm. Early coronary angiography may help to determine the relative contribution of spasm, thrombus, and underlying atherosclerotic disease.
Keywords: ecstasy; 3,4-methylenedioxymetamphetamine; acute myocardial infarction
AIM: To investigate endothelium-dependent and -independent coronary microvascular functions in patients with vasospastic angina (VSA).
METHODS: Thirty-six patients with VSA (30 men and 6 women; mean age, 58 years) were enrolled in this study. VSA was defined as ≥ 90% narrowing of the epicardial coronary arteries on angiography performed during a spasm provocation test, presence of chest pain, and/or ST-segment deviation on an electrocardiogram (ECG). Patients (n = 36) with negative spasm provocation test results and those matched for age and sex were enrolled as a control group (nonVSA group). Low-dose acetylcholine (ACh; 3 μg/min) was infused into the left coronary ostium for 2 min during the spasm provocation test. Following the spasm provocation test, nitroglycerin (0.2 mg) was administered intracoronally. Coronary blood flow (was calculated from quantitative angiography and Doppler flow velocity measurements, and the coronary flow reserve was calculated as the ratio of coronary flow velocity after injection of adenosine triphosphate (20 μg) to the baseline value. Changes in the coronary artery diameter in response to ACh and nitroglycerin infusion were expressed as percentage changes from baseline measurements.
RESULTS: Body mass index was significantly lower in the VSA group than in the nonVSA group. The frequency of conventional coronary risk factors and the rate of statin use were similar between the 2 groups. The left ventricular ejection fraction as evaluated by echocardiography was similar between the 2 groups. The duration of angina was 9 ± 2 mo. The results of blood chemistry analysis were similar between the 2 groups. Low-dose ACh did not cause coronary spasms. The change in coronary artery diameter in response to ACh was lower in the VSA group (-1.4% ± 9.3%) than in the nonVSA group (3.1% ± 6.5%, P < 0.05), whereas nitroglycerin-induced coronary artery dilatation and coronary blood flow increase in response to ACh or coronary flow reserve did not differ significantly between the 2 groups.
CONCLUSION: These findings suggest that microvascular coronary function may be preserved despite endothelial dysfunction of the epicardial coronary arteries in patients with VSA.
Coronary spasm; Endothelial function; Acetylcholine
In many patients with chest pain of esophageal origin, findings are normal on routine esophageal manometry and dysmotility develops only upon provocation with ergonovine maleate. Unfortunately, ergonovine may induce myocardial ischemia in patients in whom coronary artery spasm did not occur during previous provocative testing in a cardiac laboratory—limiting its clinical usefulness. We have recorded esophageal pressure simultaneously with ergonovine infusion during angiography in ten patients without significant arterial stenoses. In two patients their usual chest pain developed associated with esophageal spasm and without changes in coronary vessels. Simultaneous performance of angiography and manometry enhanced the diagnostic yield of provocative testing by showing esophageal motility changes. This method may detect significant changes in the esophageal motility, is easy to carry out and does not interfere with angiography. It maximizes the information gained from a single provocative test and avoids the risk of ergonovine infusion outside of a cardiac laboratory.
OBJECTIVE--To characterise clinical, investigative, and prognostic features of women referred with chest pain who subsequently underwent coronary angiography. DESIGN--Analysis of all women with angina referred to one consultant during 1987-91 who subsequently underwent coronary angiography, with follow up to present day. SETTING--Cardiothoracic centre. SUBJECTS--Women with normal coronary arteries; women with coronary artery disease shown on angiography; men with coronary artery disease matched for age; men referred with chest pain during the same period subsequently found to have normal coronary arteries. MAIN OUTCOME MEASURES--Risk factor analysis; results of exercise testing and coronary angiography; intervention; morbidity and mortality. RESULTS--Women comprised 23% (202/886) of patients referred with chest pain who subsequently underwent angiography. 83/202 women had normal coronary angiograms compared with 55/684 men (41% v 8%, P < 0.01). Diabetes mellitus was the only risk factor more frequently encountered in women with coronary artery disease (P = 0.001). The specificity and positive predictive value of exercise testing before angiography were significantly lower in women than men (71% v 93%, P < 0.001 and 76% v 95%, P < 0.001, respectively). Revascularisation procedures were as common in women with coronary artery disease as in men (81 (68%) v 70 (59%)), and there was no difference in event rate during follow up. Many patients with normal coronary arteries, irrespective of sex, had symptoms during follow up (61 (73%) women, 36 (65%) men) and continued to take antianginal drugs (27 (33%) women, 14 (28%) men); 14 (17%) women and six (11%) men required hospital readmission for severe symptoms. CONCLUSIONS--In this series, although women comprised the minority of patients referred with chest pain, a diagnosis of normal coronary arteries was five times more common in women than men. Risk factor analysis and exercise testing were of limited value in predicting coronary artery disease in women. There was no sex bias regarding revascularisation procedures, and outcome was similar. A diagnosis of non-cardiac chest pain in patients with normal coronary arteries was of little benefit to the patient with regard to morbidity.
The aim of this study is to observe the chronic effects of diltiazem release capsules on patients with coronary slow flow (CSF) phenomenon.
From 2004 to 2009, 80 consecutive patients with chest pain and normal coronary arteries evidenced by coronary angiography and CSF were included in this randomized, double-blind, placebo-controlled trial. CSF patterns were evaluated by the corrected TIMI frame count. Patients were randomly assigned at 1∶1 ratio to diltiazem sustained-release capsules treatment group (Dil, 90 mg twice daily) or placebo control group. Holter, liver and kidney function, treadmill exercise test, coronary angiography and left ventricular angiography were measured at baseline and after 6 months. The incidence of cardiovascular events (re-admission or progress in coronary heart disease, myocardial infarction, malignant arrhythmia or cardiac death) was evaluated during the 6 months follow up.
Thirty-nine patients in control and 40 patients in Dil group completed the 6 months follow-up. There was no medication induced drug withdraw during follow up. Left ventricular ejection fraction was similar between the 2 groups at baseline and during follow up. Heart rate was significantly lower in Dil group than in control group and there was no symptomatic bradycardia and II and III degree atrioventricular conduction block in both groups. Significant improvement was observed in the onset of chest pain, treadmill exercise test and coronary blood flow in Dil group while these parameters remained unchanged in control group at the end of 6 months follow up. The incidence of cardiovascular events was similar between the two groups.
Diltiazem slow-release capsules improved coronary blood flow and alleviated angina in patients with CSF.
Chinese Clinical Trial Registry ChiCTR-TCC-11001864
Coronary vasodilators have been variously reported to increase, decrease, or have no effect upon blood flow to ischemic myocardium. Consequently, the effects of two different types of dilators, nitroglycerin (TNG) and dipyridamole, were studied with radioactive microspheres in open-chested dogs after coronary artery ligation. Given as a bolus i.v. injection 0.4 mg TNG resulted in an increase in blood flow to nonischemic areas of myocardium and a preservation of flow to ischemic regions, despite a fall in blood pressure. 5 min later blood pressure and nonischemic flow were back to base line, and a small selective increase in flow to ischemic myocardium was found (0.15-0.18 ml/min per g, P less than 0.05). During an 0.2 mg/min infusion of TNG, and also after 1 mg/kg i.v. dipyridamole, ischemic flow was maintained in the face of a 20-30% reduction in blood pressure. In this setting, nonischemic flow was unchanged during TNG and doubled after dipyridamole. With the addition of methoxamine in both dilator groups, blood pressure returned to base line while flow to ischemic areas increased above base-line values (TNG, 0.16-0.20 ml/min per g, P less than 0.01; dipyridamole, 0.18-0.31 ml/min per g, P less than 0.05). Epicardial ST segment elevations increased during TNG infusion and were unchanged after dipyridamole, but with addition of methoxamine, ST segments became less elevated in both drug groups, concomitant with the observed increase in collateral blood flow. These data indicate that both types of coronary vasodilators, when used in conjunction with methoxamine to support blood pressure, reduce collateral resistance, increase collateral flow, and reduce epicardial ST-segment elevations.
The cold pressor test was used to induce myocardial ischaemia in patients with coronary artery disease and the rise in left ventricular filling pressure used as the index of myocardial ischaemia. Left ventricular filling pressure was derived from a non-invasive echophonocardiographic method. A study group of 19 consecutive patients with chest pain underwent the cold pressor test before coronary angiography. Eighteen responded with a rise in filling pressure exceeding 30% and, of these, 17 had serious coronary artery disease (three single vessel, one two vessel, and 13 triple vessel disease; one had coronary artery spasm only). The remaining patient, who showed no rise in filling pressure, did not have coronary artery disease. None of 15 normal controls showed a rise greater than 5% (patients with coronary artery disease versus normal controls p less than 0.001). The cold pressor test would be suitable for patients who cannot or should not exercise and may be combined with exercise electrocardiograms to improve the information content, as it uses a different marker of myocardial ischaemia.
Application of electrocardiogram gated digital subtraction angiography to the assessment of coronary artery bypass graft function was studied one week to eight years after bypass operation in ten unselected patients with recurrent chest pain. For the digital method, contrast was injected into the ascending aorta via a 4 or 5 French gauge catheter. The results of this technique were compared with those of selective graft and coronary angiography in the same patients by two independent observers. Of twenty six grafts in the series, patency was confirmed in twenty one by both selective and digital angiography. The quality of graft run off, graded by each observer using a simple scoring system, demonstrated six points of inter observer disagreement when standard cineangiograms were used, compared with nine points of disagreement when digital images were used. Digital subtraction angiography provided useful graft visualisation, but was less good than conventional angiography at defining the native coronary circulation. The role of this promising new technique has yet to be established.
BACKGROUND--Many studies have shown that coronary flow reserve is reduced in patients with chest pain and angiographically normal coronary arteries. The methods used to assess coronary blood flow have varied, but in nearly all reports dipyridamole has been used to bring about vasodilatation. This study was designed to assess whether the apparent impairment of coronary flow reserve seen with dipyridamole could be reproduced with either papaverine or adenosine, which induce maximum coronary blood flow by different mechanisms. METHODS--25 patients with chest pain and angiographically normal coronary arteries were studied with an intracoronary Doppler flow probe and quantitative angiography to determine epicardial coronary artery area, coronary blood flow velocity, coronary flow reserve, and coronary vascular resistance index (CVRI, the ratio of resistance after intervention to basal resistance). All patients received papaverine 8 mg. Eight patients with positive exercise tests received intracoronary papaverine (8 and 10 mg), intracoronary adenosine (6, 20, 60 micrograms), and high-dose intravenous dipyridamole (0.84 mg/kg). RESULTS--The velocity ratio (peak after intervention: baseline) (mean (SEM)) after 8 mg papaverine was 3.3 (0.2) (n = 25) and the coronary flow reserve was 4.1 (0.3) (n = 25). There were no differences between patients with a positive (n = 16) or negative (n = 9) exercise test. In eight patients coronary flow reserve was measured after increasing doses of papaverine, adenosine, and dipyridamole. Coronary flow reserve was 4.5 (0.3) with papaverine, 4.8 (0.3) with adenosine, and 3.5 (0.4) with dipyridamole (p = 0.08 v papaverine and adenosine). CVRI was 0.22 (0.01) with papaverine, 0.21 (0.02) with adenosine, and 0.29 (0.03) with dipyridamole (p < 0.05 v papaverine, p = 0.09 v adenosine). CONCLUSIONS--These results indicate that measurement of coronary flow reserve and CVRI in patients with chest pain and normal coronary arteries depends on the pharmacological stimulus. Normal values were obtained with papaverine in all patients, irrespective of the exercise test response. In patients with a positive exercise test significantly lower values were obtained with dipyridamole than with papaverine, or adenosine. The reported impairment of coronary flow reserve in patients with angina and normal coronary arteries may reflect the variability in response to different pharmacological agents. The mechanism underlying this variability is unknown, but may involve an abnormality of adenosine metabolism in the myocardium.
The cause of chest pain in patients with anomalous origin of the right coronary artery from the left sinus of Valsalva has not yet been elucidated. In the following case, this anomaly was demonstrated, upon angiography, in a patient with recurrent chest pain and a negative stress test; in addition, spasm of the left anterior descending coronary artery was documented during ergonovine provocation. To our knowledge, this is the first time coronary artery spasm has been documented in a patient with this anomaly. On the basis of this case, we recommend ergonovine testing for all angina patients with aberrant coronary arteries in whom no other cause of chest pain is found at cardiac catheterization. (Texas Heart Institute Journal 1988; 15:124-127)
Coronary vasospasm; coronary vessel anomalies; coronary circulation; angina pectoris, variant; sinus of Valsalva
The frequency and magnitude of objectively determined myocardial ischaemia during normal daily activities of patients with varying severity of coronary artery disease are unknown. Furthermore, the incidence of nocturnal resting myocardial ischaemia and frequency of coronary spasm in patients with normal coronary arteries and chest pain are also not known. One hundred consecutive patients with chest pain referred for coronary angiography were therefore investigated with exercise testing and ambulatory ST segment monitoring. Fifty two of 74 patients with significant coronary artery disease and six of 26 with no significant coronary narrowing had episodes of ST segment change during 48 hours of ambulatory monitoring. Two patients, one with normal coronary arteries and localised spasm and one with three vessel disease, had episodes of ST segment elevation, whereas all other patients had episodes of ST segment depression. The frequency, duration, and magnitude of ST segment changes were greater in patients with more severe types of coronary artery disease. Thus more than six episodes of ST segment change per day occurred in patients with two or three vessel disease or left main stem stenosis and in the only patient with coronary spasm and normal coronary arteries. Nocturnal ischaemia occurred in 15% of patients with coronary artery disease and was almost an invariable indicator of two or three vessel coronary artery disease or left main stem stenosis. Episodes of ST segment change occurred most commonly during the morning hours and least commonly during the night, in parallel with changes in basal hourly heart rates. The heart rate at the onset of ST segment change tended to be lower in patients with coronary artery disease than in those with normal coronary arteries. The duration of exercise to ST segment depression tended to be shorter in patients with more severe disease, but it could not predict patients with nocturnal myocardial ischaemia, left main stem stenosis, or coronary spasm, whereas ambulatory ST segment monitoring was able to identify most of these patients.
We report a very rare case of a 47-year-old man who had coronary spasm that resulted in a silent myocardial infarction, a ruptured myocardial wall, and a nonruptured left ventricular pseudoaneurysm. The patient presented with a 6-month history of dyspnea on exertion, without evidence of fixed coronary artery stenosis. Coronary angiography showed severe coronary spasm of the left anterior descending and left circumflex arteries; the spasm was relieved promptly by nitroglycerin. Echocardiography and left ventricular angiography revealed the large left ventricular pseudoaneurysm posterolateral to the left ventricle. We performed surgical resection of the pseudoaneurysm and patch repair of the ruptured left ventricular wall, with excellent results.
We present this case because of the highly unusual sequence of events. Early surgical intervention resulted in the patient's recovery. (Tex Heart Inst J 2002;29:122–5)
Aneurysm, false/diagnosis/surgery; coronary vasospasm; heart rupture, post-infarction/diagnosis/surgery; heart ventricle; human; male; middle age; myocardial infarction/complications
Both hypertension and coronary artery spasm (CAS) are associated with endothelial dysfunction. Thus, a higher incidence of CAS is expected in hypertensive patients. We evaluated the impact of hypertension on CAS with intracoronary acetylcholine (ACh) provocation test. A total of 986 patients (685 hypertensive patients vs 301 normotensive patients) who underwent coronary angiography with ACh provocation test were enrolled. ACh was injected into the left coronary artery in incremental doses of 20, 50 and 100 μg min−1. Significant CAS was defined as a transient >70% luminal narrowing with concurrent chest pain and/or ST-segment changes. Although the incidences of significant ACh-induced CAS were similar between hypertensive and normotensive patients (35.8 vs 39.2%, P=0.303), multivariate logistic analysis showed that hypertension was negatively associated with ACh-induced CAS (odds ratio: 0.70, 95% confidence interval: 0.51–0.94, P=0.020). The angiographic characteristics of ACh-induced CAS were similar between these two groups. Subgroup analysis regarding the impact of the status of blood pressure control on CAS showed that hypertensive patients with controlled blood pressure had a significantly higher incidence of CAS than those with uncontrolled blood pressure (45.2 vs 27.9%, P<0.001), and that uncontrolled blood pressure was negatively associated with ACh-induced CAS (odds ratio: 0.56, 95% confidence interval: 0.40–0.79, P=0.001). In conclusion, despite the expected endothelial dysfunction, hypertension and uncontrolled blood pressure are negatively associated with CAS, suggesting that the mechanisms and risk factors of CAS may be significantly different from those of coronary artery disease.
acetylcholine; coronary artery spasm; blood pressure control
Multivessel or multisegment spasm in patients with known widespread coronary atherosclerotic disease is an infrequent occurrence.
We describe a prolonged spasm of both the left main and the left anterior descending artery in a patient with chronic effort angina and multivessel coronary artery disease, who previously underwent percutaneous coronary intervention and drug eluting stents implantation. The patient complained of episodes of angina and palpitations, mainly at rest. Exercise stress test resulted positive in therapeutic wash-out. Coronary angiography was performed which showed: 80% stenosis in the proximal segment of the Left Main (LM) and the mid Left Anterior Descending artery (LAD), 90% stenosis of the Posterior Descending Artery (PDA); there was no angiographic evidence of instent restenosis in the previously stented segments. Coronary Artery By-pass Graft (CABG) was proposed, but the patient refused surgery. Reperfusion strategy included coronary angioplasty of the LM and the LAD. Before the procedure, in the presence of ischemic EKG changes, nitrates were infused in the left coronary artery with resolution of both the LM and LAD stenoses. However, intracoronary nitrates in the right coronary artery did not resolve the PDA stenosis. The patient underwent angioplasty and stenting of the PDA alone.
Selective spasm involving two anatomically different segments is rare. The left main location is critical since it can lead to unnecessary coronary artery by-pass. Intracoronary nitrates should be administered before invasive strategies are advised.
coronary artery disease; coronary spasm; intracoronary nitrates; PCI; CABG
Thromboembolism is still one of the most important complications of prosthetic heart valves. Embolism to a major coronary branch is rare, but acute proximal occlusions can be fatal, even when the coronary arteries are otherwise normal and intervention is rapid. We report a fatal complication of an exercise test in a patient who had a St. Jude bileaflet mitral valve.
After an exercise test, a 42-year-old woman with a mechanical prosthetic valve had a severe hemodynamic collapse with acute ST segment changes. Coronary angiography showed a totally occluded left main coronary artery with TIMI grade 0 to 1 flow. Rapid injection of contrast material and the passage of a floppy guidewire through the thrombus restored a TIMI grade 3 flow. Angiography showed no coronary atherosclerostic involvement. Despite successful coronary reperfusion, intra-aortic balloon counterpulsation, and intensive medication, the patient died. This case demonstrates that exercise testing should be applied with great caution in patients with prosthetic valves, and only after a careful evaluation of valve function. We recommend transesophageal echocardiography prior to exercise testing in these patients. (Tex Heart Inst J 2002;29:48–50)
Case report; coronary thrombosis/etiology; exercise test; female; heart valve prosthesis; middle age; mitral valve; myocardial infarction; prosthetic heart valves; thromboembolism/etiology
Wellens' syndrome is a pattern of electrocardiographic T-wave changes associated with critical stenosis of proximal left anterior descending artery (LAD). T-waves abnormalities were found in precordial leads, especially in V2–V3 during pain-free periods, and ECG obtained during episodes of pain demonstrates upright T-waves with possible elevated or isoelectric ST segments. Early recognition and appropriate intervention carries significant diagnostic and prognostic value. We reported a case of Wellens' syndrome with different etiology and prognosis. Although the ECG showed typical T-wave changes in V2–V5 leads, patient's coronary angiography revealed moderate stenosis in proximal LAD, and coronary artery spasm was suggested. Unlike the classic Wellens' syndrome, which needs aggressive coronary intervention, our patient fared well with conservative medical therapy (diltiazem and nitrates) and showed favorable prognosis.
Electrocardiography; Wellens syndrome; Coronary artery spasm
Background and Objectives
adial artery spasm is one of the most common complications of transradial coronary angiography (TRA): the radial artery is prone to cathecholamine-induced contraction and radial pain during TRA could increase the sympathetic tone. The object of this study was to evaluate whether the eutectic mixture of local anesthesia (EMLA) cream, in addition to lidocaine infiltration, could reduce the sympathetic response by reducing radial pain during TRA.
Subjects and Methods
Seventy-six patients were randomized 1 : 1 to either EMLA or control groups. Radial pain was measured by the visual analogue scale (VAS) and the verbal rating scale (VRS-4). Sympathetic response, including systolic (SBP) and diastolic blood pressure (DBP), pulse rate (PR), stroke volume (SV) and total peripheral resistance (TPR), was measured by photoplethysmography.
Radial pain measured during lidocaine infiltration was significantly lower in the EMLA group (VAS: 3.1 vs. 4.0, p=0.04; VRS-4: 2.0 vs. 2.2, p=0.03) and the sympathetic response was significantly blunted in the EMLA group from baseline to lidocaine infiltration (ΔSBP, mm Hg: 5 vs. 13, p<0.01; ΔDBP, mm Hg: 2 vs. 7, p=0.03; ΔPR, beat/min: 2 vs. 8, p<0.01, ΔSV, mL: 3 vs. 21, p<0.01; ΔTPR, mm Hg · L/min: 1.0 vs. 5.9, p<0.01).
In patients undergoing TRA, the EMLA cream, in addition to lidocaine infiltration, effectively reduces the radial pain and thereby the sympathetic response, during lidocaine infiltration.
Anesthesia, local; Coronary angiography; Radial artery
OBJECTIVE--To establish and compare the characteristics of older (greater than or equal to 70 years) and younger patients with chest pain selected to undergo coronary angiography and by analysis of their subsequent management to assess the value of coronary angiography for older patients with chest pain. DESIGN--Retrospective analysis of clinical case notes and coronary angiography reports. SETTING--Cardiology department with referral population of one million in an Edinburgh hospital. PATIENTS--134 consecutive patients with chest pain aged 70 years or over investigated by coronary angiography between 1978 and 1988; 134 randomly selected patients aged under 70 investigated over the same period. MAIN OUTCOME MEASURES--Clinical and angiographic features at time of angiography and management after angiography. RESULTS--Older patients represented a small, but increasing, proportion of those investigated. Older patients had more severe symptoms at the time of angiography, were taking more antianginal drugs, and had had their symptoms for longer than younger patients. At angiography more older patients had triple vessel coronary disease, left main stem stenosis, or left ventricular impairment. After angiography similar proportions of older and younger patients underwent coronary artery surgery, with more elderly patients requiring urgent operation; although operative mortality was higher for elderly patients, symptomatic benefit was similar to that in younger patients. CONCLUSIONS--Older patients with angina selected to undergo coronary angiography and subsequent coronary surgery have more severe symptoms and underlying cardiac disease. Earlier referral and investigation might yield a population with lower operative risk. Selection of patients for coronary angiography and coronary artery surgery should be based on the potential for benefit and should avoid "agism."
Although epidemiologic data link biomarkers of cardiovascular risk with incident and prevalent coronary artery disease, exact anatomic relationships between biomarkers and coronary atherosclerosis as measured by coronary CT angiography remain unclear. Patients with acute chest pain who ultimately had no evidence of acute coronary syndrome underwent contrast-enhanced 64-slice coronary CT angiography to determine presence, extent and composition of coronary atherosclerotic plaque. We determined the differences in levels of blood biomarkers measured at the time of the CT scan between different CT-based atherosclerotic plaque groups. Among 313 patients (mean age: 51.6 ± 11 years, 62% male) high-sensitivity C-reactive protein (hs-CRP) and matrix metalloproteinase-2 were associated with the extent of calcified plaque (P = 0.03 and P<0.001), while hs-CRP and apolipoprotein A1 were associated with the extent of non-calcified plaque (P = 0.03 and P = 0.004; respectively). Despite a generally lower risk profile, subjects with exclusively non-calcified plaque had significantly higher levels of hs-CRP and oxidized low-density lipoprotein (P = 0.01 and P = 0.03; respectively) and lower levels of adiponectin (P = 0.03) when compared to subjects with calcified plaque (n = 130, 42%). Biomarkers reflecting inflammation, vascular remodeling, oxidation, and lipoprotein metabolism maybe associated with different patterns of coronary atherosclerosis as quantified by coronary CT angiography.
Biomarkers; Atherosclerosis; Cardiac CT; Imaging; Coronary artery disease
Primary percutaneous coronary intervention (PPCI) is the preferred treatment method for ST elevation myocardial infarction (STEMI). However, the required equipments are not available in all hospitals. Thus, due to shortage of time, some patients receive thrombolysis therapy first. Patients with chest pain and/or persistent ST segment elevation will then undergo rescue percutaneous coronary intervention (PCI). The present study evaluated and compared the frequency of no-reflow phenomenon and 24-hour complications after PCI among patients who underwent PPCI or rescue PCI.
This cross-sectional study assessed no-reflow phenomenon, 24-hour complications, and thrombolysis in myocardial infarction (TIMI) flow in patients admitted to Chamran Hospital (Isfahan, Iran) with a diagnosis of STEMI during March-September, 2011. Subjects underwent PPCI if they had received eptifibatide. Rescue PCI was performed if patients had chest pain and/or persistent ST segment elevation despite receiving streptokinase (SK). Demographic characteristics, history of diseases, medicine, angiography findings, PCI type, and complications during the first 24 hours following PCI were collected. Data was then analyzed by Student’s t-test, chi-square test, and logistic regression analysis.
A total number of 143 individuals, including 67 PPCI cases (46.9%) and 76 cases of rescue PCI (53.1%), were evaluated. The mean age of the participants was 58.92 ± 11.16 years old. Females constituted 18.2% (n = 26) of the whole population. No-reflow phenomenon was observed in 51 subjects (37.1%). Although 9 patients (6.3%) died during the first 24 hours after PCI, neither the crude nor the model adjusted for age and gender revealed significant relations between rescue PCI and death or no-reflow phenomenon. Rescue PCI and no-reflow phenomenon were not significantly correlated even after adjustments for age, gender, history of diabetes, hypertension, hyperlipidemia, coronary artery disease, smoking, platelets number, myocardial infarction level, the extent of stenosis, and the involved artery.
According to the present study, although SK is more effective than eptifibatide in resolution of thrombosis and clots, rescue PCI did not differ from PPCI in terms of the incidence of no-reflow phenomenon or short-term complications.
Primary Percutaneous Coronary Intervention; Rescue Percutaneous Coronary Intervention; No-Reflow Phenomenon