Recurrent Episodes Of Chest Pain Research Articles

P300 ACUTE MYOCARDITIS COMPLICATED BY VENTRICULAR ARRHYTHMIAS

Abstract Background Many kinds of arrhythmias may occur in patients with myocarditis at any stage of the disease. However, as compared to the other clinical presentations, arrhythmic myocarditis has been poorly described in literature. Case Report A 20–year–old girl, without CVRF or comorbidities, presented at the ED because of palpitations and epigastric pain irradiated to left arm. 12–lead ECG evinced elevated HR and aspecific repolarization abnormalities. Blood samples showed high cTn value and normal PCR value. Echocardiography showed a preserved LVEF, without abnormalities. Patient was hospitalized with a diagnosis of suspect acute myocarditis. Following hospital stay has been complicated by recurrent episodes of chest pain with concomitant increase of cTn that finally had presented a sinusoidal trend (peak 12830ng/L). At the same time, continuous ECG monitoring has been showing frequent but short term ventricular extrasystole activity, so B–blocker therapy was optimized. On ECG monitoring, appearance of short runs of asymptomatic mono– and polymorphic NSVT and after a few days appearance of polymorphic NSVT “torsade de pointes” like, symptomatic for presyncope. New changes in kinetics appear on the echocardiogram: hypokinesia of medio–apical segments of lateral, anterior wall septum. Therapy with metoprolol and lidocaine iv was started with subsequent stabilization of the rhythm. CMR presented data suggestive of myocarditis. Patient performed several BEM at different time and centers: diagnostic signs of myocarditis were not be found. Autoimmune and infectious disease screening, abdominal echography and a PET TC total body were been performed to research a potential etiology, without positive result. Patient has been discharged with wearable defibrillator and we waited for the ICD implantation in secondary prevention. Follow–up CMR showed a resolution of inflammation and no signs of fibrosis. Blood samples did not demonstrate a rise of cTn. After discharged, she has not had news onset of ventricular arrhythmias. Conclusion The mechanisms underlying the occurrence of ventricular arrhythmias during myocardial inflammation are less clear. Arrhythmias usually being self–limited with no recurrences that follow the acute phase. Management of acute life–threatening arrhythmias is generally supportive and there is a lack of evidence to support the use of specific antiarrhythmic agents. Wearable life vest has been presented as a possible therapeutic option.

Slow Coronary Flow: Pathophysiology, Clinical Implications, and Therapeutic Management.

Coronary slow flow (CSF) is an angiographic phenomenon with specific epidemiologic characteristics, associated clinical presentation, and prognosis. Although patients with CSF are diagnosed as having "normal coronary arteries," it seems appropriate to consider CSF as a distinct disease entity requiring specific treatment. The patient with CSF is usually male, smoker, obese, with a constellation of risk factors suggestive of metabolic syndrome. Unstable angina is the most common clinical presentation, with recurrent episodes of chest pain at rest associated with electrocardiographic changes often requiring readmission and reevaluation. Regarding definition and diagnosis, interventionists should first exclude possible "secondary" causes of CSF, use objective means for definition and then differentiate from other similar conditions such as microvascular angina. Although the phenomenon is generally benign, patients with CSF are severely symptomatic with recurrent episodes of chest pain and poor quality of life. Furthermore, acute presentation of the phenomenon is commonly life-threatening with ventricular tachyarrhythmias, conduction abnormalities, or cardiogenic shock. Acute treatment of CSF includes, but is not restricted to, intracoronary infusion of dipyridamole, adenosine, or atropine. Chronic management of patients with CSF encompasses dipyridamole, diltiazem, nebivolol, telmisartan, and/or atorvastatin associated with amelioration of angina symptoms, improved quality of life, and good prognosis.

Abstract 12885: Sleepless Nights and Squeamish Days: A Conundrum of Recurrent Myocardial Ischemia

A 63-year old Caucasian female with history of aortic valve replacement and CAD with prior drug-eluting stent placement (DES) to proximal LAD and LCX, presented as a hospital transfer with recurrent episodes of chest pain. Chest discomfort was described as severe chest pressure, radiating to bilateral upper extremities. Episodes were not associated with significant exertion and frequently occurred at night/early morning. Of note, the patient had undergone coronary angiography at the outside hospital, revealing no in-stent restenosis or new coronary lesions. Soon after the patient’s arrival in the CCU, she developed profound chest pressure, accompanied by hypotension, diaphoresis and nausea. Her 12-lead ECG revealed 2-mm ST-elevation in aVR, accompanied by ST-depression in inferior, anterior, and apical leads. Initial high-sensitivity (hs)-troponin T was 26 ng/L. She was given sublingual nitroglycerin and was started on a nitroglycerin and nicardipine infusion, with resolution of symptoms after ~30 minutes, followed by normalization of hs-troponin T. A transthoracic echocardiogram did not reveal focal left ventricular (LV) wall motion abnormalities, mild LV hypertrophy was present. Given the patients’ presentation with no in-stent restenosis or new lesions, frequent episodes of chest pain-not related to exertion with occurrence at nighttime and early morning, her presentation was deemed to be consistent with epicardial coronary vasospasm. Subsequently, the patients’ anti-anginal regimen was uptitrated to include extended-release nitrates, calcium-channel blockade, and I Na blockade. Unfortunately, she continued to have frequent episodes of profound angina, accompanied by hypotension, and significant ischemic ECG changes. This prompted us to pursue bilateral sympathectomy. Subsequently, the patient had resolution of prior symptoms. She was continued on an anti-vasospastic regimen, consisting of extended release nitrates and calcium-channel blockade. This case represents the challenging management of medication-resistant epicardial coronary artery vasospasm. As previously described, sympathectomy remains an effective therapeutic option for management in these difficult and life-threatening situations.

Anomalous origin of the left coronary artery from the right aortic sinus: probably benign variant associated with a subpulmonic intramyocardial course \u2013 a case report

BackgroundAnomalous aortic origin of the left coronary artery (AAOLCA) from the right aortic sinus is a rare congenital anomaly associated with significantly increased risk of myocardial ischemia, arrhythmias and sudden cardiac death. This refers specifically to AAOLCA associated with interarterial and/or intramural course. Much less is known about anomalous origin of the left coronary artery from the right aortic sinus associated with a subpulmonic intramyocardial course.Case presentationWe report a 12 year old girl who complained of recurrent episodes of chest pain lasting for some minutes and not associated to exercise. Echocardiography revealed AAOLCA from the right aortic sinus taking a subpulmonic course within the conal septum. The diagnosis was confirmed by CT-scan and selective coronary angiography. Treadmill test, Holter-ECG and bicycle-stress echocardiography revealed no evidence of myocardial ischemia reflecting unimpaired diastolic flow in the left coronary artery. According to the nature of the complaints and in the absence of signs of myocardial ischemia the episodes of chest pain were classified as idiopathic and not associated to the coronary anomaly. We opted for a conservative approach with regular follow-up visits. During a follow-up of 2 years without restriction of sports activities the patient has been asymptomatic.ConclusionAccording to the literature AAOLCA with subpulmonary intramyocardial course appears to be associated with significantly less clinical problems than AAOLCA taking an interarterial course. The diagnosis can be suspected based on echocardiography and confirmed by contrast-enhanced computed tomography. Until now there are only few data concerning the natural history and incidence of complications in this specific anomaly. Despite the probably benign nature we recommend regular follow-up examinations including stress-testing in these patients.

42. Large vessel vasculitis with rapidly expanding aortic aneurysm

IntroductionThis case report describes the delay in diagnosis and potentially life-threatening complications of a patient with large vessel vasculitis.The initial diagnosis was of vascular Ehlers-Danlos Syndrome, based on family history and imaging. However, recurrent episodes of chest pain and a rapidly expanding aortic aneurysm prompted further diagnostics which led to the diagnosis of giant cell arteritis with large vessel vasculitis. The patient required thoracic surgery due to expansion of the aortic aneurysm. This case demonstrates the risk of delaying the diagnosis of large vessel vasculitis and the complexities of immunosuppression in the context of major surgery.Case descriptionA previously fit and well 69-year-old man presented with constitutional symptoms and intermittent chest pain for six months. Two months after symptom onset, he was admitted with chest tightness and shortness of breath. He had raised inflammatory markers with thrombocytosis and was given antibiotics for a probable chest infection.A CT pulmonary angiogram revealed ascending aorta dilatation, 47mm with wall thickening. The radiologist reported this as being most likely due to systemic hypertension. There was no evidence of malignancy on abdominal and pelvic imaging. The aortic changes were attributed to possible underlying Ehlers-Danlos syndrome, as his daughter had a diagnosis of Ehlers-Danlos Type III. He was discharged despite persistently raised inflammatory markers and no positive microbiology.He was readmitted after six weeks with pyrexia and severe chest pain. A CT of his thoracic aorta showed further expansion of the aortic aneurysm, 59mm with a slightly thickened abdominal aorta wall. With a rapidly expanding aortic aneurysm and persistent raised inflammatory markers, the suspicion of large vessel vasculitis was raised. No symptoms of cranial temporal arteritis or polymyalgia rheumatica. A FDG-PET scan showed high uptake in the ascending, thoracic and upper abdominal aorta in keeping with extra-cranial large vessel vasculitis. He was treated with IV methylprednisolone for three days with subsequent oral prednisolone. Whilst on high dose glucocorticoids, he developed steroid induced diabetes and hypomania hence oral methotrexate 15 mg once weekly was added.The cardiothoracic team elected to delay cardiothoracic surgery until he was on less than 15 mg of oral prednisolone daily. However, reduction of oral prednisolone led to a flare of giant cell arteritis. The patient had to undergo elective aortic valve and ascending aorta replacement whilst on 40 mg of prednisolone. Tocilizumab was added two months after surgery and prednisolone was successfully reduced to 3mg.DiscussionCritically, appropriate treatment was delayed due to misdiagnosis of Ehlers-Danlos Syndrome; this was largely based on the family history. This red herring likely distracted clinicians from seeking a better explanation for the patient’s presentation and aortic changes.The initial oral steroid course was complicated by steroid induced complications and pending cardiothoracic surgery. The surgical team planned to delay surgery until the patient is on a lower prednisolone dose, due to the increased risk of infection and poor wound healing. The patient therefore had a rapid steroid tapering regime, reducing by 5mg two-weekly, from a starting oral dose of 65mg. Such rapid steroid tapering carries a risk of disease flare, and in fact two weeks prior to surgery, his inflammatory markers rose, and his prednisolone dose had to be increased from 25mg to 40mg.A collaborative decision between the rheumatologists and surgeons was then made to proceed with surgery despite the high-dose steroids, as simultaneous inflammation control and prompt surgical repair took precedence over the potentially increased post-operative risks.The patient also experienced steroid-related side-effects, but the switch to steroid-sparing agents was challenging. Starting tocilizumab as a further immunosuppressant had to be delayed until after surgery, as IL-6 inhibition would distort C-reactive protein as a measure of both disease activity and potential post-operative infection.In summary, this case highlights the difficulty in diagnosing large vessel vasculitis and the potential delay in treatment can cause significant morbidity and mortality.Appropriate imaging is crucial to ascertain a diagnosis of large vessel vasculitis. Immunosuppression must be tailored individually, accounting for side-effects and competing risks.Points for discussion include the use of newer imaging modalities in diagnosing large vessel vasculitis and monitoring disease activity. The efficacy and safety of tocilizumab as a steroid-sparing agent for this condition should also be investigated.Key learning pointsThe importance of early diagnosis and treatment in patients with large vessel vasculitis, as vascular complications can arise if treatment is delayed.The use of appropriate imaging modalities such as MR angiogram and FDG-PET is crucial for diagnosis of large vessel vasculitis.Glucocorticoid therapy is the mainstay treatment for large vessel vasculitis, but side-effects can be limiting. Steroid sparing agents, such as IL-6 inhibitors should be considered early as an alternative immunosuppressant for patients with large vessel vasculitis.Careful planning of immunosuppression is required prior to major surgery.Conflicts of interestThe authors have declared no conflicts of interest.

Anomalous Aortic Origin of Left Coronary Artery Leading to Sudden Cardiac Arrest in Young Female

Purpose: Anomalous aortic origin of the coronary artery(AAOCA) is an uncommon but important cause of sudden death in young patients. Vigilance is required to ascertain a prompt diagnosis and expedite surgery to prevent further fatal events. We describe a case of a 20-year-old female with an anomalous left coronary artery origin, whose presentation and path to diagnosis and treatment is outlined. Methodology: A 20-year-old female presented following an out of hospital cardiac arrest (OOHCA) whilst swimming. ROSC was achieved with CPR and a single defibrillation from an AED. History revealed recurrent episodes of chest pain and syncope over the previous 4 years. She was evaluated 3 years prior by cardiology; TTE and EST were found to be normal and EP review for prolonged QTS stratified her as a low risk for QTS. She was discharged without further investigations. CTCA performed following her arrest revealed an anomalous left coronary artery, arising from the right coronary sinus, passing intramurally between the aortic root and pulmonary trunk. This was repaired by deroofing the left coronary artery across the top of the left and right commisure of the aortic valve. The aortic valve commisure was re-suspended with good outcome. Results: Surgery provided excellent immediate results and exercise stress test at 6 months was negative. She remained asymptomatic with no further episodes of chest pain or syncope and is now able to perform strenuous activities. Conclusion: The AAOCA arising from the opposite sinus of Valsalva is a rare but an important condition which targets children and adolescents with an often fatal outcome if diagnosis is missed.

Chest Pain: The Need to Consider Less Frequent Diagnosis

Chest pain is one of the most frequent patient's complaints. The commonest underlying causes are well known, but, sometimes, in some clinical scenarios, it is necessary to consider other diagnoses. We report a case of a 68-year-old Caucasian male, chronically hypertensive, who complained of recurrent episodes of chest pain and fever with elevated acute phase reactants. The first investigation was negative for some of the most likely diagnosis and he quickly improved with anti-inflammatory drugs. Over a few months, his symptoms continued to recur periodically, his hypertension was aggravated, and he developed headaches and lower limbs claudication. After a temporal artery biopsy that was negative for vasculitis, he underwent a positron emission tomography suggestive of Takayasu Arteritis. Takayasu Arteritis is a rare chronic granulomatous vasculitis of the aorta and its first-order branches affecting mostly females up to 50 years old. Chest pain is experienced by >40% of the patients and results from the inflammation of the aorta, pulmonary artery, or coronaries.

Double hazards of ischemia and reperfusion arrhythmias in a patient with variant angina pectoris

Variant angina pectoris, also called Prinzmetal’s angina, is a syndrome caused by vasospasms of the coronary arteries. It can lead to myocardial infarction, ventricular arrhythmias, atrioventricular block and even sudden cardiac death. We report the case of a 53 year-old male patient with recurrent episodes of chest pain and arrhythmias in the course of related variant angina pectoris. It is likely that the reperfusion following myocardial ischemia was responsible for the ventricular fibrillation while the ST-segment returned to the baseline. This case showed that potential lethal arrhythmias could arise due to variant angina pectoris. It also indicated that ventricular fibrillation could be self-terminated.

A Rare Cause of Chest Pain and Ventricular Fibrillation

Aman in his late 50s presented with sudden-onset chest pain followedbyashockfromhis implantablecardioverter-defibrillator (ICD). His history included a cardiac arrest secondary to ventricular fibrillation resulting in ICD implantation 1yearprior, chronicobstructivepulmonarydisease,hypertension,andactivetobaccoandalcoholabuse. Therewas no history of hyperlipidemia or family history of coronary arterydisease.His initial symptomwasparesthesia in the righthand, whichprogresseduphisarmandwasfollowedbychest tightnessand dyspnea.Notably,hehad6similarpresentations intheprecedingyear, butmyocardial infarction hadbeen ruled out by serial electrocardiograms (ECGs) and cardiac biomarker results on all occasions. On arrival to the hospital, his blood pressure was 109/77 mmHg, heart ratewas 66 beats/min, and blood oxygen saturation was97%while breathing roomair. Hewas admitted to thehospital and received3 additional shocks fromhis ICD in the emergencydepartment. EachshockwasprecededbychestpainandECGchanges that resolved after administration of sublingual nitroglycerin. One of theseECGs is shown inFigure 1,whichprompted immediatecoronary angiography. Questions: What is the etiology of his chest pain? Why did his ICD fire? Patient Course Coronary angiography showed no obstructive coronary artery disease, with only a 30% stenosis in his circumflex coronary artery. Initial views showed diffuse vasospasm of both the right and left coronary arteries, which resolved with administration of intracoronary nitroglycerin (Figure 2). Tests for serum creatine kinase and troponin T had negative results. His lipid panel results were notable for total cholesterol of 127 mg/dL and low-density lipoprotein cholesterol of 67 mg/dL (to convert to millimoles per liter, multiply by 0.0259). Interrogation of the ICD revealed 4 episodes of ventricular fibrillation with appropriate treatment (Figure 3), each preceded by chest pain. He received a diagnosis of coronary vasospasm leading to ventricular fibrillation and was treated with a statin, antiplatelet therapy, long-acting nitrate, and amlodipine besylate (dihydropyridine class of calcium channel blockers). He continued to have recurrent episodes of chest pain and ST-segment elevation while receiving amlodipine, so he was switched to verapamil hydrochloride (phenylalkylamine class of calcium channel blockers), after which he had no recurrence of chest pain or ST-segment elevation on ECG. He was exhorted to cease tobacco and alcohol use and discharged home.

Intracardiac Fistulae: A Rare Complication of Infective Endocarditis

We present the case of a diabetic gentleman who was admitted to the hospital with an infected right foot. Swabs were positive for Staphylococcus aureus and Pseudomonas aeruginosa. His right big toe was amputated. Postoperatively, the patient experienced recurrent episodes of chest pain. He was therefore transferred to the coronary care unit, where he deteriorated rapidly. The patient was subsequently transferred to intensive care. Transthoracic and transesophageal echocardiograms revealed evidence of aortic dissection, but this finding was not confirmed in a computed tomography scan. The patient subsequently experienced cardiac arrest and died. The postmortem examination revealed no aortic dissection but did show a vegetation on the mitral valve with a fistula that tracked into a ruptured epicardium.

Recurrent pericarditis caused by transdiaphragmatic migration of surgical tacks

A 61-year-old man was investigated because of recurrent episodes of chest pain, the first of which had occurred shortly after undergoing endoscopic abdominal hernia repair. At that time, resting electrocardiogram (ECG) and cardiac troponin had been repeatedly normal, and pulmonary embolism had been excluded. Because of recurrent symptoms …

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.

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

AN ATYPICAL CASE OF TYPICAL CHEST PAIN

A 68-year-old woman presented to emergency department(ED) for a 2-week history of fatigue and recurrent episodesof chest pain on exertion described as constrictive andassociated with dyspnea. The duration of each episode ofpain was about 30 min. To relieve her symptoms, she usedtransdermic and sublingual nitrates with no benefit.The past medical history revealed primary biliarycirrhosis diagnosed in 1994, a celiac syndrome and anonsteroidal antiinflammatory-induced gastropathy. Shehad also a long-standing history of Raynaud’s phenome-non, arthritis, sclerodactily and positive anticentromereantibodies. There was no history of coronary artery diseaseand no risk factor for cardiovascular diseases. Homemedication were omeprazole, NSAID, and ursodeoxy-cholic acid.On general examination the patient was afebrile andmildly bradycardic (56 beats/min). The blood pressure was110/60 torr. Pulmonary, cardiac, and abdominal examina-tions revealed no abnormalities. No oedema was observedin the lower limbs. An enlarged thyroid was palpable.The differential diagnosis of chest pain in a patient withknown connective tissue disorder is extensive, rangingfrom benign to life-threatening etiologies.Musculoskeletal chest wall pain is a common etiology,particularly in rheumatic diseases due to frequentinvolvement of thoracic joints. This kind of pain is oftenlocalized and positional; it may be exacerbated by deepbreathing, turning, and arm movement.Ischemic pain due to coronary artery disease has to becarefully considered as a cause of chest discomfort inpatients with connective tissue disorders. This issue wasemphasized in previous studies [1, 2] that show increasedrisk of cardiovascular events in connective tissue disorders,particularly in rheumatoid arthritis and erythematosussystemic lupus. The ischemic disease does not appear to bemediated through traditional risk factors, but may be theresult of chronic inflammation associated with endothelialdysfunction and a hypercoagulable state [3].The presence of a pleuritis or a pericarditis has to beexcluded in our patient, since serositis is common in con-nective tissue disorders. Pericardial pain is typically suddenin onset, and occurs over the anterior chest. It may beexacerbated by inspiration, and may decrease in intensitywhen the patients sits up and leans forward.Also the presence of pulmonary hypertension has to beruled out in initial evaluation of chest pain. This chroniccondition is due to abnormalities in pulmonary vessels thatare frequent in patients with rheumatoid arthritis, systemicerythematosus lupus, and systemic sclerosis. In this setting,chest pain is typically associated with exertional dyspneaand seems to be related both to pulmonary artery stretchingand to right ventricular ischemia.The chest pain may also be related to an esophagealdisease, particularly in our patient who had clinical featuresof limited cutaneous systemic sclerosis. Esophagealhypomotility and reduction in the lower-esophagealsphincter tone are common in patients with systemicsclerosis [4]. These motility abnormalities may result ingastroesophageal reflux and reflux esophagitis. Gastro-esophageal reflux disease may cause symptoms similar toangina pectoris, including a sensation of chest pressureradiating to the neck and arms, which can be triggered byphysical exercise and emotions, and relieved by nitrate

An atypical case of typical chest pain

A 68-year-old woman presented to emergency department(ED) for a 2-week history of fatigue and recurrent episodesof chest pain on exertion described as constrictive andassociated with dyspnea. The duration of each episode ofpain was about 30 min. To relieve her symptoms, she usedtransdermic and sublingual nitrates with no benefit.The past medical history revealed primary biliarycirrhosis diagnosed in 1994, a celiac syndrome and anonsteroidal antiinflammatory-induced gastropathy. Shehad also a long-standing history of Raynaud’s phenome-non, arthritis, sclerodactily and positive anticentromereantibodies. There was no history of coronary artery diseaseand no risk factor for cardiovascular diseases. Homemedication were omeprazole, NSAID, and ursodeoxy-cholic acid.On general examination the patient was afebrile andmildly bradycardic (56 beats/min). The blood pressure was110/60 torr. Pulmonary, cardiac, and abdominal examina-tions revealed no abnormalities. No oedema was observedin the lower limbs. An enlarged thyroid was palpable.The differential diagnosis of chest pain in a patient withknown connective tissue disorder is extensive, rangingfrom benign to life-threatening etiologies.Musculoskeletal chest wall pain is a common etiology,particularly in rheumatic diseases due to frequentinvolvement of thoracic joints. This kind of pain is oftenlocalized and positional; it may be exacerbated by deepbreathing, turning, and arm movement.Ischemic pain due to coronary artery disease has to becarefully considered as a cause of chest discomfort inpatients with connective tissue disorders. This issue wasemphasized in previous studies [1, 2] that show increasedrisk of cardiovascular events in connective tissue disorders,particularly in rheumatoid arthritis and erythematosussystemic lupus. The ischemic disease does not appear to bemediated through traditional risk factors, but may be theresult of chronic inflammation associated with endothelialdysfunction and a hypercoagulable state [3].The presence of a pleuritis or a pericarditis has to beexcluded in our patient, since serositis is common in con-nective tissue disorders. Pericardial pain is typically suddenin onset, and occurs over the anterior chest. It may beexacerbated by inspiration, and may decrease in intensitywhen the patients sits up and leans forward.Also the presence of pulmonary hypertension has to beruled out in initial evaluation of chest pain. This chroniccondition is due to abnormalities in pulmonary vessels thatare frequent in patients with rheumatoid arthritis, systemicerythematosus lupus, and systemic sclerosis. In this setting,chest pain is typically associated with exertional dyspneaand seems to be related both to pulmonary artery stretchingand to right ventricular ischemia.The chest pain may also be related to an esophagealdisease, particularly in our patient who had clinical featuresof limited cutaneous systemic sclerosis. Esophagealhypomotility and reduction in the lower-esophagealsphincter tone are common in patients with systemicsclerosis [4]. These motility abnormalities may result ingastroesophageal reflux and reflux esophagitis. Gastro-esophageal reflux disease may cause symptoms similar toangina pectoris, including a sensation of chest pressureradiating to the neck and arms, which can be triggered byphysical exercise and emotions, and relieved by nitrate

Diffuse vascular calcification in a dialysis patient

CASE PRESENTATION A 35-year-old Hispanic male on hemodialysis for end-stage renal disease (ESRD) secondary to diabetic nephropathy was admitted with chest pain and shortness of breath. The chest pain was localized to the midline, without any radiation or diaphoresis and was present at rest. The patient was bed-bound due to bilateral below-knee amputations. He had recurrent episodes of chest pain and shortness of breath in the past 3 months for which he was hospitalized. During these admissions, his cardiac enzymes were within normal limits. A stress test performed recently was technically limited, but showed a small inferior defect with normal left ventricular function. He had a past history of type I diabetes mellitus since the age of 10. Subsequently, he developed peripheral neuropathy, blindness secondary to retinopathy, nephropathy with ESRD, and underwent below-knee amputation of left and right limbs for severe peripheral vascular disease 6 and 12 years before, respectively. He had no history of cerebrovascular accident. He also had a past history of hypertension and hypercholesterolemia. His medications included lisinopril, metoprolol, nifedipine, aspirin, clopidogrel, and insulin. He had a strong family history of diabetes, with his mother and brother being diabetes patients. On physical examination, he was lethargic, afebrile with a blood pressure of 170/86 mm Hg, heart rate of 70 beats per minute, respiratory rate of 14 breaths per minute with an oxygen saturation of 97% on 21 of supplemental oxygen, and jugular venous pressure of 14cm. Cardiac examination revealed audible S3 and S4. Respiratory examination revealed fine rales at the left lung base and decreased breath sounds at the right lung base. His tunneled catheter site on the right side of the neck was clean, with no tenderness or erythema. The remainder of the systemic examination was unremarkable.

Delayed stenting of a thrombotic saphenous vein graft after intravenous tirofiban pretreatment

Percutaneous intervention of thrombus containing lesion carries a high risk of periprocedural complications [1]. If the culprit lesion is a saphenous vein graft, thrombus burden is usually large [2]. Optimal treatment strategy for such situation is still not well-defined. We describe a staged approach with intravenous tirofiban infusion prior to stent implantation for the management of a large thrombus in a stenosed old vein graft. A 66-year-old man with a history of previous inferior MI, was admitted to our hospital because of recurrent episodes of chest pain at rest. Risk factors were hypertension, non-insulin-dependent diabetes and smoking. Eight years earlier he underwent a coronary angiography that revealed severe three-vessels disease. Coronary artery bypass graft was performed with a sequential saphenous vein graft to first diagonal and first marginal branch and a left internal mammary artery to left anterior descending coronary artery; the right coronary artery of small caliber, was not grafted. After four years the patient had a non ST-elevation myocardial infarction and underwent stenting of the circumflex artery. He remained asymptomatic for four years under medical therapy up to the current admission. On admission the ECG showed T wave inversion in lateral leads. There was a mild increase in total creatine kinase up to 270 IU/l. At coronary angiography the left internal mammary artery graft was patent with diffuse disease in the distal left anterior descending, the right coronary artery was occluded proximally with moderate in-stent restenosis of the

Cardiac Toxicity Associated with Capecitabine Therapy

Cardiac Toxicity Associated with Capecitabine Therapy

Clustering of Recurrent Pericarditis With Effusion and Constriction in a Family

To describe a cluster of cases of pericarditis in a midwestern family of German and Danish ancestry. Retrospective review of available medical records identified 5 family members in 2 generations with confirmed diagnosis of pericarditis. Five family members, 3 males and 2 females, presented for medical evaluation of recurrent chest pain between 1969 and 1991. Physical examination resulted in the diagnosis of pericarditis with effusive and constrictive features. The age at presentation ranged from 8 to 46 years. Despite extensive investigations, an idiopathic etiology was assigned to each case. In follow-up, all 5 family members had recurrent episodes of chest pain, self-limiting or responsive to medical therapy, but the effusive component remained a notable feature of the syndrome. Diagnosis of pericarditis in 5 family members may represent the first description of familial clustering of isolated pericarditis. In addition, 3 other family members had symptoms of chest pain, but pericarditis remained undiagnosed. The aggregate history suggests autosomal dominant inheritance with incomplete penetrance.

Value of navigator echo magnetic resonance angiography in detecting occlusion/patency of arterial and venous, single and sequential coronary bypass grafts.

Aim of our work was to validate magnetic resonance angiography (MRA) in detecting occlusion/patency of coronary artery bypass grafts. Twenty patients with previous history of bypass surgery and recurrent episodes of chest pain were enrolled. Two patients could not be studied (claustrophobia, erratic breathing). Thus, 18 patients with 51 bypasses were examined using a navigator echo sequence: 21 arterial grafts (six sequential) and 30 saphenous vein grafts (five sequential). All patients had undergone contrast conventional angiography 3-15 days before MRA. The magnetic resonance (MR) data set was analyzed by two independent readers blinded to the results of conventional angiography (occlusion of 12 of 51 grafts). At magnetic resonance, two bypasses of the posterior descending artery, patent at conventional angiography, could not be visualized because of imaging slab malpositioning. Interobserver concordance was 96% (47/49). Magnetic resonance and conventional angiography provided identical answers in 47 out of 49 (96%) of the examined grafts. Eleven out of 12 occluded grafts and 36 out of 37 patent grafts were correctly identified with MR. As far as occlusion is concerned, the sensitivity of MR was 91%, the specificity 97%. To summarize, a 30 min outpatient MR examination is highly reliable in determining occlusion/patency of arterial and venous, single and sequential bypasses.