Episodes Of Chest Pain Research Articles

Cardiac Myxoma Showing Extramedullary Hematopoiesis in a Patient with Beta Thalassemia

A 52-year-old woman presented with recurrent episodes of chest pain, shortness of breath, palpitations, and fatigue for three months. Her past medical history was significant for chronic anemia. Physical examination revealed a pansystolic murmur radiating to the left axilla. Her admission workup showed microcytic anemia. Her serum creatinine and iron studies were within normal limits and her hemoglobin electrophoresis pattern was that of beta thalassemia minor. Two-dimensional echocardiography showed a multilobulated mobile mass attached to the mitral annulus at the base of the anterior mitral valve leaflet. The patient underwent surgical resection of the mass. Pathology examination revealed a cardiac myxoma with conspicuous foci of extramedullary hematopoiesis.

Plasma nociceptin/orphanin FQ levels rise after spontaneous episodes of angina, but not during induced myocardial ischemia

The aim of our study was to evaluate the effects of repeated episodes of angina and induced myocardial ischemia on plasma nociceptin/orphanin FQ (N/OFQ) levels. Patients with unstable angina (23 with new onset severe angina or accelerated angina and 18 with subacute angina at rest) who had had repeated spontaneous episodes of chest pain in the last week before the study underwent myocardial perfusion single-photon emission computed tomography using adenosine infusion. Twenty subjects without clinical symptoms of angina matched for age, sex and cardiac risk factors served as a control group. N/OFQ levels were significantly ( P < 0.01) higher in the patients (15.2 ± 2.1 pg/ml) than in the control group (8.5 ± 2.6 pg/ml). Blood pressure and heart rate did not significantly differ. All patients showed transient adenosine infusion myocardial ischemia that did not induce chest pain or significantly modify plasma N/OFQ levels or hemodynamic parameters. Our findings show that unstable angina is associated with a significant increase in circulating N/OFQ levels unrelated to intervening transient myocardial ischemia or hemodynamic changes. This increase is probably related to the chest pain repeatedly occurring in the course of coronary artery disease, but absent during transient adenosine-induced myocardial ischemia.

A Case of Excessive Yawning With Citalopram

A Case of Excessive Yawning With Citalopram

Safety of contrast flash-replenishment stress echocardiography in 500 patients with a chest pain episode of undetermined origin within the last 5 days

Safety concerns regarding the use of echo-contrast agents during baseline and SE in patients with recent chest pain have been raised. The purpose of the present study was to provide evidence regarding the safety of flash-replenishment contrast dipyridamole-atropine echocardiography (DASE) in such patients. Five hundred consecutive individuals who presented to the Emergency Department with chest pain, normal electrocardiograms (ECG) and troponin I were selected based on a less than 5 days interval between chest pain episode and performance of contrast flash-replenishment DASE. Analysis of myocardial perfusion with SonoVue infusion after dipyridamole was routinely added on top of standard wall motion assessment during DASE. Adverse events (AEs) were reported according to standardized terminology and then compared with a historical control group in which contrast was not used. No deaths, myocardial infarctions, sustained arrhythmias, or any other life-threatening events were observed. Adverse events were not significantly different between the study group and the control group. In the selected subgroup of patients (n = 149) who underwent coronary angiography, accuracy of DASE with additional perfusion assessment was higher (88%, 95% C.I. 83-93%) than without (72%, 95% C.I. 65-79%). DASE with SonoVue infusion for myocardial perfusion assessment was exceptionally safe even when routinely performed within the first 5 days following a chest pain episode of undetermined origin in subjects without ECG and troponin abnormalities.

A large saphenous vein graft aneurysm one year after coronary artery bypass graft surgery presenting as a left lung mass

Aneurysm of a saphenous vein graft (SVG) is a rare but fatal complication of coronary artery bypass graft (CABG) surgery. The development of SVG aneurysms appears usually about 10-20 years after the operation at an estimated rate of <1%. A 68-year-old male was referred to the emergency department after frequent episodes of dyspnea, chest pain and hemoptysis. He previously had CABG surgery one year before. The physical examination was normal. Chest radiogram showed a left pulmonary midzone mass. CT-angiogram demonstrated a large aortic pseudoaneurysm (6.36 x 6.06 cm) in the middle part of the ascending aorta. After sternotomy, the ascending aorta above sinotubular junction near the origin of brachiocephalic artery was resected and replaced with a tube graft. The patient was transferred to ICU with stable hemodynamic status. SVG aneurysm should be considered while encountering mediastinal mass or undiagnosed cardiopulmonary symptoms in patients with a previous history of CABG because of its rarity and overlap of symptoms with other thoracic, pulmonary, and cardiac diseases. Surgery seems to be the treatment of choice to reduce the risk of rupture and embolism.

Rapid assessment of rest myocardial ischaemia in the Chest Pain Unit

A 76-year-old man with a history of coronary bypass graft surgery presented to the Chest Pain Unit with chest discomfort. He underwent myocardial perfusion imaging (MPI) with 99m Tc-sestamibi. Immediately after acquisition of the rest scan he developed a new chest pain episode and received an additional tracer injection. The new images showed hypoperfusion in the inferior and inferolateral walls that were not observed in the previous rest scan images (a arrows). A coronary angiogram revealed subtotal proximal occlusion of a saphenous vein graft to the right coronary artery (b arrow) which was submitted to successful stent implantation. Acute coronary syndrome results from the combination of intermittent thrombotic occlusion and vasoconstriction resulting in markedly decreased regional myocardial perfusion [1]. Abnormal rest MPI in patients with acute chest pain is highly associated with acute myocardial infarction or the need for subsequent coronary revascularization [2]. These images demonstrate the exquisite sensitivity of MPI to changes in rest myocardial perfusion over a short period.

Muscular Ventricular Septal Defect Visualized as Nonreversible Perfusion Abnormality on Myocardial Perfusion SPECT and Confirmed on Cardiac Computed Tomography Angiography Images

A 47-year-old woman with no history of CAD presented with an episode of left-sided atypical chest pain. Her work-up was negative for acute MI. She underwent a myocardial perfusion Tc-99m tetrofosmin SPECT study to rule out myocardial ischemia. The SPECT images revealed a small nonreversible mid-anteroseptal perfusion defect. For additional evaluation coronary computed tomography angiography was performed. This revealed normal coronary arteries and demonstrated a small muscular ventricular septal defect which corresponded to the location of the fixed perfusion defect on the SPECT images. The presence of the ventricular septal defect should be considered in differential diagnosis of an isolated fixed septal perfusion abnormality on SPECT images in patients with no history of prior MI.

Type 1 ST-segment elevation in the right precordial leads associated with acetylcholine-induced localized spasm of the conus branch of the right coronary artery

A 61-year-old man with a history of frequent and early-morning episodes of chest pain was referred to our hospital for evaluation of coronary artery disease. He had no family history of Brugada syndrome or sudden cardiac death. Resting 12-lead electrocardiogram (ECG) showed no abnormality of ST-T wave. After admission, he underwent coronary angiography with written informed consent. The patient had no significant lesions of the major coronary artery and branches at baseline. Acetylcholine (ACh) injection into the left coronary artery induced coronary spasm in the proximal portion of the left anterior descending artery.

Unusual case of left ventricular ballooning involving the inferior wall: a case report

BackgroundTako – tsubo like syndrome (also named left ventricular apical ballooning) is an unusual cardiomyopathy with an high incidence in Japanese population of female sex, following an emotional stress. The clinical features (typical chest pain), and the electrocardiographic changes (negative T wave and persistent ST elevation in anterior leads), are suggestive of an acute myocardial infarction; nevertheless the coronary angiography show coronary arteries without lesions and the ventriculography show specific segmental dysfunction. In the literature there are many reports of typical left ventricular ballooning (apical); due to the rarity of the atypical localizations (such as mid, basal, anterior or inferior left ventricular wall) many authors think they are different physiopatologic entity.Case reportWe report a case of 50 – years old woman, with a family history of ischeamic cardiomyopathy but with no additional cardiovascular risk factors, who arrived to emergency department with a recent episode of chest pain (about 30 minutes) with electrocardiographic and echocardiographic features suggested of a inferior ST elevation myocardial infarction. Coronary angiography showed coronary arteries without atherosclerotic lesions; ventriculography showed an inferior dysfunction.ConclusionThis data can suggest for an atypical form (in term of clinical presentation and localization) of left ventricular ballooning involving the inferior wall (never described in the literature), not preceded by any emotional or physical stress. The follow – up performed by transthoracic echocardiography (2 months later) revealed a complete regression of wall motions abnormalities.

Therapeutic Development in Cardiac Syndrome X: A Need to Target the Underlying Pathophysiology

Morbidity of patients with cardiac syndrome X (typical anginal-like chest pain and normal coronary arteriogram) is high with continuing episodes of chest pain and frequent hospital readmissions. Management of this syndrome represents a major challenge for the treating physician. Conventional therapies with antianginal agents such as nitrates, calcium channel antagonists, classic beta-adrenoceptor blockers and nicorandil have been tried, with variable success. However, this might be related to a failure to target the underlying pathophysiology and, clearly, more effective therapies are needed. Supporting evidence for the important role of endothelial dysfunction and oxidative stress in the pathogenesis of cardiac syndrome X has come from the recent observation that basal superoxide production predicts future cardiovascular events in this patient group. This review will discuss the pathophysiology, current medical management and potential new pharmacological treatment for patients with cardiac syndrome X which target endothelial dysfunction and oxidative stress. What's already known about this topic? Morbidity of patients with cardiac syndrome X is high. The important role of endothelial dysfunction and oxidative stress in the pathogenesis of cardiac syndrome X. What does this article add? This review will discuss the pathophysiology, current medical management and potential new pharmacological treatment for patients with cardiac syndrome X which target endothelial dysfunction and oxidative stress.

Anomalous coronary sinus drainage into the left atrium

1934-5925/$ -see front matter 2009 doi:10.1016/j.jcct.2008.12.008 A 57-year-old woman with hypertension and hyperlipidemia but without known coronary artery disease underwent prospective-gated 64-row computed tomography coronary angiography (CTCA) because of an episode of atypical chest pain. The axial images showed anomalous drainage of the coronary sinus (CS) into the medial aspect of the posterior wall of the left atrium (LA). The right cardiac vein emptied directly into the right atrium (Fig. 1). Multiplanar reformatted images clearly showed the slightly tortuous CS coursing to the LA, and its anatomic relation with the cardiac chambers (Fig. 2). Three-dimensional virtual angioscopic image of the LA showed the pulmonary veins ostia and an additional, elliptical ostium in the medial aspect of the posterior wall, corresponding to the anomalous drainage of the CS. Congenital anomalies of the coronary sinus are rare, and include complete absence, hypoplasia, narrowing, atresia, partial or complete unroofing, and fistula from a persistent left superior vena cava. Knowledge of coronary venous structure and morphology is particularly clinically important

Unexpected Coexisting Myocardial Infarction Detected by Delayed Enhancement MRI

We report a case of an unexpected coexisting anterior myocardial infarction detected by delayed enhancement MRI in a 41-year-old man following a presentation with a first episode of chest pain during inferior acute myocardial infarction. This second necrotic area was not initially suspected because there were no ECG changes in the anterior leads and the left descending coronary artery did not present any significant stenoses on emergency coronary angiography. Unrecognised myocardial infarction may carry important prognostic implications. CMR is currently the best imaging technique to detect unexpected infarcts.

Peri-procedural Anticoagulation and the Incidence of Haematoma Formation after Permanent Pacemaker Implantation

1474 pts. 902 pts were admittedwith ACS, of whom 274 pts were transferred from another hospital. We analysed the 628 ACS admissions from the ACH catchment area. Results: 208 pts were admitted with a STEMI, 331 pts a NSTEMI and 89 pts with unstable angina pectoris (UAP). Themean agewas 66.1± 13.7 years, 395 (62.9%)weremale. The total number of tpn T tests performedwas 1811, mean 2.9 (SD1.1), median 3(IQR 2-3), with a range of 1–8 tests per pt. If 2 testshadbeenperformedperpt, as recommendedby theNZACSGuidelines,wewouldhave seen 1256 tests at a cost of $15,687. In fact, we found that there were 1811 tests performed, at a total cost of $22,619, an extra cost to the CCUof$6932overa13month timeperiod. 381patientshad > 3 tpn tests performed. (We have not taken into account pts who had further episodes of chest pain on the CCU.) Conclusion: Unnecessary blood tests performed in the CCU are costly in a constrained health service. We found that 555 ‘extra’ tpn T testswere performed over a 13month time period. More judicious use of blood tests would have a significant cost saving for a hospital. doi:10.1016/j.hlc.2009.05.229

Chest Pain without Significant Coronary Stenosis after Implantation of Sirolimus-Eluting Stents

We encountered a case of exercise-induced chest pain after the implantation of sirolimus-eluting stents (SESs). She had no history of previous chest pain, and an exercise stress test just after the implantation of the SESs was negative without any symptoms. However, six months after the implantation of the SESs, she began to experience frequent episodes of severe chest pain on effort in spite of there being no significant coronary stenosis. Interestingly, severe coronary vasoconstriction was induced by an intracoronary administration of acetylcholine, and exercise stress testing revealed positive findings with chest pain and ST-T segment depression on ECG. An intensive treatment with two types of calcium channel blockers could readily and completely abolish the exercise-induced chest pain and ST-T segment depression on the ECG. In view of these findings, we presumed that coronary microvessel dysfunction and/or exercise-induced coronary vasoconstriction leading to myocardial ischemia had appeared 6 months after the implantation of the SESs. Although the pathogenesis of this phenomenon could not be completely elucidated, the anatomical and functional abnormalities of the coronary arteries associated with the implantation of the SESs may have been one of the most important mechanisms.

Very Late Thrombosis of a Drug-Eluting Stent After Discontinuation of Dual Antiplatelet Therapy in a Patient Treated With Both Drug-Eluting and Bare-Metal Stents

Drug-eluting stents (DESs) are the treatment of choice for obstructive coronary artery disease when percutaneous intervention is feasible. However, late stent thrombosis seems to occur more frequently with DESs and is closely associated with the discontinuation of dual antiplatelet therapy. We report a case of very late stent thrombosis after discontinuation of dual antiplatelet therapy. The patient suffered from acute myocardial infarction (MI) and underwent bare metal stent (BMS) implantation in the left anterior descending artery (LAD) five years prior to presentation. Three years after BMS implantation, he presented again with acute MI and had a DES implanted in the right coronary artery (RCA). He ran out of his medication, but failed to refill his prescription. Sixteen days after discontinuing medication, he experienced an episode of chest pain and was taken to the cardiac catheterization laboratory, where he was found to have thrombosis in the DES, but no thrombosis in the BMS. It is possible that DESs are more vulnerable to late thrombosis than are BMSs, supporting the use of prolonged dual antiplatelet therapy in patients treated with DESs. The patient was successfully treated with balloon angioplasty and thrombus aspiration without complications.

Bad cable, good cable

A 23-year-old female with history of smoking but otherwise no significant medical history presented with recurrent episodes of chest pain. An electrocardiogram (EKG) was performed, which showed T-wave inversion in leads V1 and V3 but not V2. There was also an abnormal Rwave progression with an abnormally prominent R wave in lead V2 (Fig. 1), raising the suspicion of leads V2 and V3 reversal. Switching cables did not fix the problem. Because this was suspected to be most likely artifactual, a different EKG machine was used with a more reasonable R-wave progression (Fig. 2). Upon inspection by a biomedical consultant, the cable on the first machine was found to be malfunctioning, with lead (V2) shorting with the ground and was subsequently replaced. It was thought that, with frequent use of the EKG machine, not uncommon practice in a cardiology office, the actual current generated, although

Type B aortic dissection in a patient with unknown left ventricular non-compaction cardiomyopathy: Cardiovascular magnetic resonance diagnosis

A 61-year-old man was referred at our hospital for a cardiac evaluation after an episode of oppressive chest pain at rest. He was discharged with a MRI diagnosis of non-compaction cardiomyopathy presented with typical angina, left ventricle dysfunction and ischemic EKG findings without atherosclerotic narrowing and also with a type B aortic dissection, documented also by computed tomography.

Incomplete Longitudinal Ventricular Septal Fracture After Blunt Chest Trauma

A currently asymptomatic 31-year-old man was referred for recent atypical short stabbing chest discomfort occurring at rest. One month earlier, he had complained of a prolonged chest pain episode lasting ≈1 day, temporally related to the use of inhaled cocaine, for which he did not seek medical consultation. He had smoked half a pack of cigarettes a day for 15 years and suffered 2 remote episodes of blunt chest trauma. The first occurred at 12 years of age when he was in a low-velocity automobile accident as a …

Vasospasm-induced polymorphic ventricular tachycardia

A 63-year-old man was admitted for workup of syncope and episodic, midsternal chest pain of one-year duration. During another episode of chest pain after admission, the electrocardiogram (Figure 1) revealed a heart rate of 55 beats/min; ST elevation in leads II, III and aVF; with reciprocal ST depression in leads I and aVL and upsloping ST depression in leads V1 to V4, demonstrating inferior and posterior wall myocardial ischemia. The telemetry rhythm strip (Figure 2) revealed ST elevation followed by wide-complex polymorphic ventricular tachycardia at 300 beats/min, characteristic of torsades de pointes that resolved 5 min later. Cardiac enzymes were within normal limits. Transthoracic echocardiography showed no ventricular dysfunction or wall motion abnormalities and cardiac catheterization revealed no evidence of stenotic coronary artery disease. These findings demonstrate polymorphic ventricular tachycardia in the setting of variant or Prinzmetal’s angina in the absence of obstructive coronary artery disease (1). The patient was subsequently treated with felodipine and a nitroglycerin patch to prevent episodes of variant angina, and reported no further episodes in six months of follow-up (2). Figure 1) Electrocardiogram revealing a heart rate of 55 beats/min; ST elevation in leads II, III and aVF, with reciprocal ST depression in leads I and aVL and upsloping ST depression in leads V1 to V4, demonstrating inferior and posterior wall myocardial ischemia ... Figure 2) Telemetry rhythm strips revealing ST elevation followed by wide-complex polymorphic ventricular tachycardia at 300 beats/min, characteristic of torsades de pointes that resolved 5 min later. Strip 1 Vasospasm; Strip 2 Polymorphism; Strip 3 Normal sinus ...

Scintographic Evidence of Severe Myocardial Hypoperfusion in a Patient With Left Anterior Descending Coronary Artery Bridging—Case Report and Review of the Literature

Myocardial bridging is a congenital abnormality characterized by an intramyocardial course of a major epicardial coronary artery segment. Generally considered a benign condition, myocardial bridging has been associated with angina, acute myocardial infarction, and sudden death. Herein, we report a patient with an intramyocardial segment in the mid portion of the left anterior descending coronary artery with marked systolic compression. Single photon emission computed tomography with technetium-99m tetrofosmin done to evaluate an episode of chest pain showed a large predominantly fixed perfusion defect in the mid to apical anterior wall with partial reversibility. The patient's chest pain did not recur and repeat single photon emission computed tomography imaging 14 days later with rest-redistribution thallium-201 showed normal myocardial perfusion. The overall clinical impression was that myocardial bridging resulted in severe transient anterior myocardial hypoperfusion. The literature on prevalence, diagnosis, use of perfusion imaging, and hemodynamic effects of myocardial bridging is reviewed.