Induced Chest Pain Research Articles

Acute aortic dissection during scuba diving

ABSTRACT Yanagawa Y, Ohsaka H, Yatsu S, Suwa, S. Acute aortic dissection during scuba diving. Undersea Hyperb Med. 2024 Second Quarter; 51(2):185-187. A 60-year-old man with hypertension and dyslipidemia complained of chest pain upon ascending from a maximum depth of 27 meters while diving. After reaching the shore, his chest pain persisted, and he called an ambulance. When a physician checked him on the doctor’s helicopter, his electrocardiogram (ECG) was normal, and there were no bubbles in his inferior vena cava or heart on a portable ultrasound examination. The physician still suspected that he had acute coronary syndrome instead of decompression illness; therefore, he was transported to our hospital. After arrival at the hospital, standard cardiac echography showed a flap in the ascending aorta. Immediate enhanced computed tomography revealed Stanford type A aortic dissection. The patient obtained a survival outcome after emergency surgery. To our knowledge, this is the first reported case of aortic dissection potentially associated with scuba diving. It highlights the importance of considering aortic dissection in patients with sudden-onset chest pain during physical activity. In addition, this serves as a reminder that symptoms during scuba diving are not always related to decompression. This report also suggests the usefulness of on-site ultrasound for the differential diagnosis of decompression sickness from endogenous diseases that induce chest pain. Further clinical studies of this management approach are warranted.

TCTAP C-197 Optical Coherence Tomography Defined Plaque Erosion After Removal of Coronary Guidewire

### Patient Initials or Identifier Number CGP ### Relevant Clinical History and Physical Exam A 45 years-old man visited outpatient room with exercise induced chest pain. Chest pain developed during climbing 3 months ago and occurred during exercise for 30 minutes on the day of visit. He had no

Manifestation of J wave induced by acetylcholine applied for a coronary spasm provocation test in a patient with aborted sudden cardiac death

A 51-year-old man with a resuscitation episode was referred to our hospital. Coronary angiography revealed a focal spasm overlapped with organic stenosis where a bare metal stent was implanted. Acetylcholine (ACh) provocation test did not induce chest pain. It revealed no discernible ST-T changes but unmasked a J wave at the end of the QRS complex, which was associated with short-coupled repetitive premature ventricular beats. A J wave reportedly appears immediately before the onset of ventricular fibrillation caused by vasospastic angina. However, a J wave observed newly after a coronary spasm provocation test using ACh without ST-T changes is informative when considering the mechanisms of the J wave.

Tender Endothelium Syndrome: Combination of Hypotension, Bradycardia, Contrast Induced Chest Pain, and Microvascular Angina.

Hypotension, bradycardia, and contrast induced chest pain are potential complications of cardiac catheterization and coronary angiography. Catheter-induced coronary spasm has been occasionally demonstrated, but its relationship to spontaneous coronary spasm is unclear. We describe a 64-year-old female who underwent coronary artery bypass surgery in 1998 on the basis of an angiographic diagnosis of severe left main disease, who recently presented with increasingly frequent typical angina. Repeat coronary angiography was immediately complicated by severe chest pain, hypotension, and bradycardia but demonstrated only mild disease of the left main artery and entire coronary tree with complete occlusion of her prior grafts. This reaction was almost identical to that observed during her original coronary angiogram. We now believe her original angiogram was complicated by severe catheter-induced left main spasm, with the accompanying contrast reaction attributed to left main disease, and the occlusion of coronary grafts explained by the absence of significant left main disease. The combination of these symptoms has not been documented in the literature. In this instance, these manifestations erroneously led to coronary bypass surgery. It is unknown whether routine, systematic injection of intracoronary nitroglycerin prior to angiography might blunt the severity of such reactions.

Early use of beta blockers in patients with cocaine associated chest pain

BackgroundThe most common symptom of cocaine abuse is chest pain. Cocaine induced chest pain (CICP) shares patho-physiological pathways with the acute coronary syndromes (ACS). A key event is the increase of activity of the adrenergic system. Beta blockers (BBs), a cornerstone in the treatment of ACS, are felt to be contraindicated in the patient with CICP due to a potential of an “unopposed alpha adrenergic effect (UAE)”. ObjectivesIdentify signs of UAE and in-hospital complications in patients who received BB while having cocaine induced chest pain. MethodsWe performed a retrospective review of 378 patients admitted to a medical unit because of CICP. Twenty six of these were given a BB at the time of admission while having CICP. We compared these patients to a control group paired by age, sex, race and history of hypertension who did not received a BB while having CICP. Blood pressure, heart rate, length of stay and in-hospital cardiovascular complications were compared. ResultsNo statistically significant differences were found between the two groups except for a longer length of stay in the case group. This was felt to be due to unrelated causes. ConclusionsThis study does not support the presence of an UAE in patients with continuing CICP and treated early with BB. There were no in-hospital cardiovascular complications in the group of patients who had an early dose of BB while having CICP. ImplicationsBB appeared safe when given early on admission to patients with CICP.

Retrosternal Heartburn in Division I Athlete

HISTORY: A 20-year-old African American collegiate basketball forward presented with retrosternal “heartburn” to the athletic training staff during practice. He was given antacids which seemed to help and he went home to rest. On awakening, the retrosternal pain was persistent and increased in severity. He presented to the hospital complaining of worsening retro-sternal chest pain. The onset was sudden with squeezing sharp sensation, associated with diaphoresis. Pain was worse with sitting up; improving while lying down and with inspiration. He denied radiation, shortness of breath, palpitations, dizziness or syncope. He received aspirin and pain medication, decreasing his pain from 8/10 to 2/10. PHYSICAL EXAMINATION: Physical exam revealed the following vitals: BP 137/73, Pulse 46, Temp 96.4 F, Respiratory rate 20, Height 6’4”, weight 214 lbs, BMI 26.13, and SpO2 100%. He appeared non-toxic. No carotid bruit or JVD were appreciated on examination. His chest wall was non-tender to palpation. Auscultation: regular bradycardia without murmurs, rubs, or gallops. No Marfanoid features. The remainder of the examination was normal. DIFFERENTIAL DIAGNOSIS: 1.Angina 2.Gastroesophageal reflux 3.Drug induced chest pain 4.Pneumonia/pneumonitis/pulmonary contusion 5.Acute NSTEMI 6.Pericardial effusion TEST AND RESULTS: Chest x-ray negative for acute process Drug screen + Troponin 14.39 EKG: sinus bradycardia with early repolarization TIMI Score 2 Echocardiogram: Ejection Fraction 55-60% with 1 cm globular mass attached to the P1 scallop of the posterior leaflet of the mitral valve. This was found to be mobile on the atrial side. Cardiac catheterization: Normal Left main and RCA without stenosis. Pending labs at discharge included Anti-phospholipid anti-bodies and ANA. FINAL/WORKING DIAGNOSIS: NSTEMI secondary to mitral valve myxoma emboli TREATMENT AND OUTCOMES: 1. He was transferred from the local hospital to a Cardiac Center 2. He underwent minimally invasive cardiothoracic surgery. 3. Cardiac rehabilitation over 12 weeks; clearance for return to play Division 1 basketball. 4. Recommended cessation of tobacco use.

Causes systémiques ou originales de douleurs thoraciques

Takotsubo syndrome can rarely lead to ‘broken heart’ death. It is probably linked to spasms of coronary arteries induced by stress. Extensive akinesia of the heart apex has been demonstrated together with focal myocardial oedema on MRI and transient lower voltage of QRS on EKG. Several drugs like cocaine, high dose morphine, metamphetamine and cannabis can also induce coronary spasms, as well as some chemotherapies for cancer. Kounis syndrome, including de novo angina in young people together with various allergic features, can follow exposure to contrasts agents or other allergizing products. Right endocarditis leads to painful septic emboli in the lungs. Spontaneous dissections of coronary arteries rarely occur in post-partum, as well as isolated sub-clavian dissections in young women. Pain in basithoracic left flank worsened by exercise associated with transient haematuria is suggestive of nutcracker syndrome due to pinching of left renal vein between aorta and superior mesenteric artery. Hypercalcaemia and hypocalcaemia, carpal tunnel syndrome, and various disorders of dorsal back or spinal cord can also induce chest pain, as well as sternal infections and numerous costal tumours. Auto-inflammatory syndromes (mainly FMF and TRAPS), and various connectivitis and vasculitis can also foster thoracic pain: lupus, rheumatoid arthritis, rheumatoid vasculitis, granulomatous vasculitis, Kawasaki's disease, Behçet, sarcoidosis, polychondritis, IgG4 syndrome, hypereosinophilic syndromes, pulmonary fibrosis, as well as various types of porphyrias and Fabry's disease.

CRT-69 Non Invasive Evaluation Of Cocaine Induced Chest Pain Reduces Cost Compared To Invasive Strategy

Evaluate the effect of invasive (IT) and non-invasive treatment (NIT) modalities on hospitalization cost and readmission rate in patients admitted with cocaine induced chest pain (CICP). As cocaine use has become more widespread, the number of cocaine-related cardiovascular events and cost of care

The value of exercise treadmill test in evaluation of coronary artery disease

Objective: To evaluate the value of Exercise treadmill test (ETT) in the diagnosis of coronary artery disease (CAD). Methods: Here we reviewed 142 (men, 104, mean age, 52.7±8.6) consecutive patients admitted to the 4th Clinical Hospital of Harbin Medical University for suspicion of CAD and they underwent ETT before coronary angiography (CAG). Patients were divided into four groups to see the sensitivity of different ETT criteria: group I: ETT negative, group II: ETT positive (ST-segment depression ≥0.1mv for more than 2 minutes), group III: ETT positive (exercise induced chest pain), group IV: ETT positive (exercise induced chest pain and ST-segment depression). The severity of coronary artery stenosis was assessed by CAG, only those with >50% of narrowing in at least one of the three major arteries or their first-order branches was considered CAG positive. Results: The false negative rate was 30.6% and the accuracy rate was 69.4% in group I. In group II, III and IV, the accuracy rates and false positive rates were 53.7% and 46.3%, 78.6% and 21.4%, 86.7% and 13.3%, respectively, (p<0.05). Furthermore, we analyzed the data of male patients in each group and the accuracy rates were 67.9%, 60.7%, 76.9%, 100%, respectively, (p<0.05). Multivariate logistic regression results showed that ST-segment depression together with exercise induced chest pain were the most related factors in CAD diagnosis. Conclusion: ST-segment depression and exercise induced chest pain are the strongest factors in CAD diagnosis. Chest pain combined with ST-segment depression had a much higher accuracy rate than ST-segment depression alone.

“Perseverant Heart”

“Perseverant Heart”

The Utility of Treadmill Testing in Children with Exercise Induced Chest Pain

The Utility of Treadmill Testing in Children with Exercise Induced Chest Pain

Outcomes of Patients With Cocaine Induced Chest Pain in An Inner City Hospital.

BackgroundCocaine induced chest pain is a major reason for admission in Safety Net Hospitals in the United States. The majority of patients admitted undergo extensive work-up leading to enormous economic burden. We hypothesize that in individuals with low risk, cocaine does not further increase adverse cardiovascular outcomes.MethodsWe conducted a retrospective chart review of all patients admitted with chest pain to our hospital between 07/01/09 and 06/30/10. We excluded patients with modifiable risk factors for coronary artery disease (CAD). The study population was divided into cocaine and non-cocaine group based on urine drug screen. We analyzed data including demographic, laboratory, cardiac testing, detection of CAD, length of stay and mortality rates.ResultsA total of 426 individuals matched our inclusion and exclusion criteria and were considered to have no known modifiable cardiac risk factors; 54 in cocaine group and 372 in non-cocaine group. Based on physician discretion, 41(76%) in the cocaine group and 239(64%) in the non-cocaine group underwent various modalities of cardiac testing. Cardiac testing was positive in 6(2.5%) patients in non-cocaine group and none in the cocaine group (p=0.597). There was no significant difference between length of stay and in-hospital mortality between the two groups.ConclusionsIn individuals at low risk for CAD, cocaine use resulted in higher rate of cardiac testing. However, there is no difference in prevalence of CAD and in-hospital mortality between the two groups. We conclude that cocaine does not increase adverse outcomes in patients with low risk for CAD.

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.

Dobutamine stress test and beta-agonist - a potential concern for nuclear cardiology testing: a case report

IntroductionChest pain with ST-segment elevation is a rare clinical problem during dobutamine stress testing. Although beta-agonists treatment prior to dobutamine stress testing has been shown to reduce the duration and amount of dobutamine infusion and atropine requirement, there is insufficient information about potential complications of this pharmacologic combination.Case presentationWe present a 67-year-old patient with dobutamine stress testing -induced chest pain and ST elevation who received albuterol for clinical treatment of bronchospastic disease prior to the test. She developed persistent chest pain and ST elevation despite medical management. Urgent cardiac catheterization showed no significant obstructive coronary artery disease. Thus coronary artery spasm was likely responsible for the chest pain and electrocardiogram abnormality in our patient as a result of β-agonist and dobutamine combination.ConclusionsBeta-agonists pre-treatment with dobutamine stress testing may induce coronary spasm in association with chest pain and ST elevation. Clinicians and nuclear cardiologist should be aware of this potential side effect of β-agonists treatment with dobutamine stress testing, particularly since dobutamine stress testing in nuclear cardiology is done in patient with chronic obstructive lung disease.

2.6

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Oral magnesium therapy, exercise heart rate, exercise tolerance, and myocardial function in coronary artery disease patients

Background: Previous studies have demonstrated that in patients with coronary artery disease (CAD) upward deflection of the heart rate (HR) performance curve can be observed and that this upward deflection...

Vocal cord dysfunction concurrent with a nutcracker esophagus and the role of gastroesophageal reflux disease

Psychological disorders were originally thought to be the sole cause of vocal cord dysfunction (VCD). Subsequently, other organic diseases, including structural laryngeal abnormalities, have also been reported to be associated with VCD. To describe the first patient with VCD concurrent with a nutcracker esophagus and to establish the association between VCD and gastroesophageal reflux disease (GERD) by using the Bernstein test. Symptom assessments, neuropsychiatric evaluations, fiberoptic laryngoscopy, pulmonary function tests, allergic skin prick tests, radiographs of the chest and sinuses, esophageal manometry (including 24-hour ambulatory esophageal pH monitoring), and the Bernstein test were performed. A 36-year-old woman had dyspnea, hoarseness, chest pain, and wheezes without relief for a decade. Neuropsychiatric evaluations disclosed mild depression. Fiberoptic laryngoscopy showed posterior laryngitis and paradoxical vocal cord adduction with audible inspiratory stridor. Pulmonary function tests showed attenuation of the inspiratory limb with notching in both flow-volume loops and a mid-vital capacity expiratory to inspiratory flow ratio of 4. All the symptoms except chest pain were improved dramatically by speech therapy and empirical treatment for GERD. Esophageal manometry revealed a nutcracker esophagus; 24-hour ambulatory esophageal pH monitoring demonstrated multiple short reflux episodes. The Bernstein test was conducted, and all the manifestations were reproduced with 0.1 N hydrochloric acid but not with isotonic sodium chloride infusion. This is the first human case report confirming that GERD can trigger an acute attack of VCD and may induce chest pain as a nutcracker esophagus in patients with VCD. It strengthens this association and expands our knowledge of diverse manifestations of this clinical entity.

A prospective, randomized, controlled trial of benzodiazepines and nitroglycerine or nitroglycerine alone in the treatment of cocaine-associated acute coronary syndromes

The purpose of the present study was to compare the use of lorazepam plus nitroglycerine (NTG) versus NTG alone in the reduction of cocaine induced chest pain in the emergency department. The secondary objective of the study was to help determine the safety of lorazepam in the treatment of cocaine- associated chest pain. The study was a prospective, randomized, single-blinded, controlled trial conducted at an university-affiliated urban emergency department (ED). All patients who presented with cocaine-associated chest pain were enrolled. Exclusion criteria included age greater than 45 years, documented coronary artery disease, chest pain of more than 72 hours duration, or pretreatment with nitroglycerin. Patients were given either sublingual nitroglycerine (SL NTG) (Group 1) or SL NTG plus 1 mg of lorazepam intravenously (Group 2) every 5 minutes for a total of 2 doses. Chest pain was recorded on an ordinal scale of 0 to 10 at baseline, and then at 5 minutes after each dose. Adverse reactions to medication were also recorded. Twenty-seven patients met the inclusion criteria and were enrolled in the study. The average age of these subjects was 34.1 years, and 67% were men. The NTG-only group consisted of 15 patients and the NTG-plus-lorazepam group consisted of 12 patients. Baseline mean chest-pain scores were 6.87 in Group 1 and 6.54 in Group 2, with no differences between groups. Five minutes after initial treatment, mean scores for the two groups were 5.2 and 3.9, respectively, with a difference in means of 1.24 (95% confidence interval [CI] −0.8-3.8). Five minutes after the second treatment, the mean scores were 4.6 and 1.5, respectively, with a difference in means of 3.1 (95% CI 1.2-5). Kruskal-Wallis testing showed a significant difference in pain relief between the two study groups (P =.003), with greater pain relief noted at 5 and 10 minutes in the NTG-plus-lorazepam group (P =.02 and P =.005, respectively). All patients in the study were admitted to the hospital, but no patient in either group had an acute myocardial infarction or cardiac complications in the ED. No adverse side effects were noted for either group. The early use of lorazepam with NTG was more efficacious than NTG alone, and appears to be safe in relieving cocaine-associated chest pain. (Am J Emerg Med 2003;21:39-42. Copyright 2003, Elsevier Science (USA). All rights reserved.)

Cardiovascular manifestations of pheochromocytoma

Pheochromocytomas are rare tumors that originate in chromaffin tissue and produce their distant variant effects by secretion of catecholamines, tending to mislead the emergency physicians to a wrong diagnosis. Therefore, we analyze the clinical cardiovascular manifestations in patients with pheochromocytoma to improve the diagnostic ability of the emergency physicians. All patients presenting to the Chang Gung Memorial Hospital between January 1993 and December 1997 with a final diagnosis of pheochromocytoma had their charts reviewed. The data of 25 patients including age, sex, adrenergic stimulation presentations, electrocardiographic changes, location of the tumor, and complications were analyzed. Hypertension was the most important major manifestation and fluctuation of blood pressure drew our attention to the possibility of pheochromocytoma. Six patients had abnormal electrocardiographic ST-T segment changes. Five of them had chest pain which prompted them to undergo coronary angiography before surgery, because acute coronary syndrome (unstable angina and acute myocardial infarction) was suspected initially. However, all of them turned out to have normal coronary arteries. Right-sided pheochromocytoma was found in three of these five patients. We should maintain high index of suspicion for pheochromocytoma in patients presenting with chest pain, fluctuating blood pressure, and ischemic electrocardiogram (ECG) changes despite any typical isoenzyme changes. Pheochromocytoma should also be included in the differential diagnosis of acute coronary syndrome because acute catecholamine secretion may induce chest pain and abnormal ECG changes mimicking an ischemic episode. The right-sided pheochromocytoma may present more striking electrocardiographic abnormalities and clinical manifestations. (Am J Emerg Med 2000;18:622–625.

Baroreflex sensitivity in the elderly with silent myocardial ischemia

In order to assess high-pressure barocepture sensitivity and parasympathetic function in elderly patients with silent myocardial ischemia, we selected 45 inpatients in our geriatric unit for a prospective cohort study of patients with coronary heart disease. All patients were over 65 years of age (37 men and 8 women) and had coronary heart disease, documented by an angiographic study and electrocardiographic evidence of myocardial ischemia during exercise stress testing, performed according to the Bruce protocol. The subjects were divided in three subgroups: group 1 (22 patients) with electrocardiographic and echocardiographic history of myocardial infarction but no angina chest pain during exercise testing; group 2 (13 patients) with no exercise induced chest pain; and group 3 (10 patients) with exercise-induced chest pain. Baroceptor sensitivity was assessed in all subjects, by evaluating heart rate changes expressed in RR interval on the basis of changes in the mean arterial pressure during intravenous infusion of stepwise doses (50–100 and 150 μg) of phenylephrine hydrochloride. Heart rate changes were also evaluated during overshoot of the Valsalva maneuver (Valsalva max.), providing an index of parasympathetic activity. Our results showed that group two patients (only silent ischemia) had significantly ( P>0.001) greater baroceptor sensitivity than the other two groups (group 2; 15.2±1.9 ms/mmHg; group 1: 10.0±1.7 ms/mmHg; and group 3: 9.8±1.7 ms/mmHg). Group two also showed a significant positive correlation ( r=0.58; P<0.05) between baroceptor sensitivity and end-diastolic pressure and a significant inverse correlation ( r=−0.672; P<0.05) between baroceptor sensitivity and the ejection fraction. Group 2 patients had a significantly longer RR interval than group 1 ( P<0.05) and group 3 ( P<0.05); a significant positive correlation ( r=0.620; P<0.05) between Valsalva max. and end-diastolic pressure; and a significant inverse correlation ( r=0.694; P<0.05) between Valsalva max. and the ejection fraction. Valsalva max. and baroceptor sensitivity correlated significantly in all three groups (group 1, r=0.707; P<0.001; group 2, r=0.94; P<0.001; and group 3; r=0.833; P<0.05). In conclusion our data suggest that elderly patients with silent ischemia appear to have an increased capacity for evoking parasympathetic reflexes that could inhibit pain perception.