Development Of Chest Pain Research Articles

Myocarditis in monkeypox-infected patients: a case series

ObjectivesMonkeypox, a zoonotic orthopoxvirus, has spread to many countries in recent months, involving mostly men who have sex with men with multiple partners. Clinical presentation includes skin lesions, systemic signs, and less frequent skin superinfections or anorectal and ophthalmic involvements. We aim to detail cases of myocarditis attributable to monkeypox, an entity that has been poorly described. MethodsThis is a descriptive case series reporting three cases of myocarditis that occurred in patients infected with monkeypox in France in 2022. ResultsPatients were adult men with no medical history who had skin lesions with positive polymerase chain reaction for monkeypox virus. A few days after the onset of cutaneous signs, patients developed acute chest pain, elevated cardiac markers, and biological inflammatory syndrome compatible with myocarditis. Two patients presented electrocardiogram abnormalities and decreased ejection fraction associated with kinetic disturbances on transthoracic electrocardiography. The last patient had normal transthoracic electrocardiography and normal electrocardiogram, but cardiac magnetic resonance imaging showed segmental inferolateral acute myocarditis. Patients were hospitalized and received cardioprotective treatment. One received antiviral treatment with tecovirimat. Symptoms and laboratory abnormalities rapidly resolved in all patients. DiscussionThese cases suggest an association between monkeypox infections and cardiac inflammatory complications. The development of chest pain in an infected patient should not be underestimated and should lead to prompt investigations for myocarditis. Monkeypox infection should also be included in the differential diagnosis of myocarditis, particularly in at-risk patients such as men who have sex with men with multiple partners in whom complete examination for skin or mucosal lesions should thus be performed.

A humanized anti‐cocaine mAb blocks the cardiovascular effects of cocaine in rats

Cocaine use and abuse is associated with significant morbidity and mortality. Further, its use has significant effects on cardiovascular function in humans and has been associated with development of chest pain, myocardial ischemia and in rare cases cardiac death. Currently, the FDA has no approved pharmacotherapy for cocaine abuse. We have developed and generated a humanized anti‐cocaine monoclonal antibody (mAb), h2E2, which dramatically decreases brain cocaine concentrations by sequestering cocaine in the plasma. As h2E2 proceeds into clinical trials, a significant question remains as to whether the increased plasma cocaine concentrations, increased circulation time of cocaine, and the decrease in cocaine excretion into the urine affects cardiac function. Therefore, the objective of this study was to determine the dose, duration and effects of cocaine administration in the presence and absence of mAb h2E2 on echocardiographic variables in an in vivo rat model.Echocardiography was performed on Sprague‐Dawley rats with indwelling catheters using the Vevo 2100 ultrasound machine with a 20mHz probe. Baseline echocardiographic long axis M‐mode images were collected prior to an i.v. cocaine push and at subsequent time points thereafter. Initial studies determined the dose‐dependent effect of cocaine on cardiac parameters including ejection fraction (EF), heart rate (HR) and cardiac output (CO). The most significant increase in EF was observed with 1.68mg/kg cocaineHCl, which was then used in the subsequent experiments.As noted, cocaine administration increased EF, with inversely proportional changes in left ventricular systolic volume. In addition, cocaine produced an immediate decrease in HR, which did not fully return to baseline over the 45 minute time course, likely due to the anesthesia, as the saline control group demonstrated comparable effects. Similarly, cocaine caused an immediate decrease in CO, which normalized over time.Pre‐administration of a single equimolar dose of h2E2 significantly blunted the effect of cocaine on EF, including both the initial drop as well as the subsequent increase. At one week and one month post h2E2, there was no significant blunting of the increased in cocaine‐induced inotropy. However, the initial decrease in EF was still blocked after one week. The initial cocaine‐induced drop in HR was blocked by h2E2, even at 1 week post‐injection. h2E2 similarly blocked the increase in CO, however this effect was not detectable after 1 week or 1 month.In conclusion, there were no significant adverse cardiac effects noted with h2E2 administration and co‐administration with cocaine resulted in significant blunting of both cocaine’s inotropic and chronotropic effects. Elevated plasma cocaine concentrations are pharmacologically inert in the presence of h2E2.

Unusual dyspnea in a hemodialysis patient: A case report

The typical clinical symptoms of hemothorax include a rapid development of chest pain or dyspnea, which may be life-threatening without immediate management. As we know, spontaneous hemothorax, a collection of blood within the pleural cavity without previous history of trauma or other cause, which usually onsets suddenly. The early and accurate diagnosis of spontaneous hemothorax is imperative in clinical practice. We reported a middle-age male undergoing regular hemodialysis was referred to our emergency department due to unknown cause of dyspnea and acute respiratory failure. Chest radiography revealed bilateral patchy infiltration of lung. Pleural tap analysis showed exudative pleural effusion with numerous red blood cells. Video-assisted thoracic surgery (VATS) were performed and confirmed the final diagnosis of spontaneous hemothorax. He was then successfully treated with the surgery of VATS combined chest tube thoracostomy.

Exaggerated hypertensive response to exercise and myocardial ischemia in patients with known or suspected coronary artery disease

ObjectivesThe association between an exaggerated hypertensive response to exercise (EHRE) and the probability of ischemia in stress tests is controversial. Our purpose was to determine the possible association between an EHRE and the development of chest pain and electrocardiographic or echocardiographic ischemia with exercise. Patients and methodsA retrospective observational study was conducted of 10,047 patients with known or suspected coronary artery disease referred for exercise echocardiography. A logistic regression analysis assessed the effect of developing an EHRE (defined as a maximum systolic blood pressure with exercise ≥220mmHg) and the onset of chest pain and electrocardiographic and echocardiographic changes suggestive of ischemia. ResultsA total of 402 patients developed an EHRE. The rates of angina, electrocardiographic ischemia and echocardiographic ischemia among the patients with an EHRE were 8.2, 16.2 and 22.6% versus 13.8, 14.7 and 27.5%, respectively, for patients without an EHRE (p=.001, p=.4, p=.032). After a multivariate fit, EHRE was associated with a lower probability of exercise-induced angina (OR, 0.44; 95% CI 0.30–0.65; p<.001) and echocardiographic ischemia (OR, 0.63; 95% CI 0.48–0.83; p=.001) but not with the onset of electrocardiographic ischemia. ConclusionsEHRE is associated with a lower prevalence of angina and echocardiographic ischemia in patients with known or suspected coronary artery disease.

Respuesta hipertensiva exagerada al ejercicio e isquemia miocárdica en pacientes con enfermedad coronaria conocida o sospechada

ObjectivesThe association between an exaggerated hypertensive response to exercise (EHRE) and the probability of ischaemia in stress tests is controversial. Our purpose was to determine the possible association between an EHRE and the development of chest pain and electrocardiographic or echocardiographic ischaemia with exercise. Patients and methodsA retrospective observational study was conducted of 10,047 patients with known or suspected coronary artery disease referred for exercise echocardiography. A logistic regression analysis assessed the effect of developing an EHRE (defined as a maximum systolic blood pressure with exercise ≥220mmHg) and the onset of chest pain and electrocardiographic and echocardiographic changes suggestive of ischaemia. ResultsA total of 402 patients developed an EHRE. The rates of angina, electrocardiographic ischaemia and echocardiographic ischaemia among the patients with an EHRE were 8.2, 16.2 and 22.6% versus 13.8, 14.7 and 27.5%, respectively, for patients without an EHRE (p=.001, p=.4, p=.032). After a multivariate fit, EHRE was associated with a lower probability of exercise-induced angina (OR, 0.44; 95% CI 0.30-0.65; p<.001) and echocardiographic ischaemia (OR, 0.63; 95% CI 0.48-0.83; p=.001) but not with the onset of electrocardiographic ischaemia. ConclusionsEHRE is associated with a lower prevalence of angina and echocardiographic ischaemia in patients with known or suspected coronary artery disease.

Platitudes and Attitudes.

Platitudes and Attitudes.

Allgrove syndrome: an Egyptian family with two affected siblings

BackgroundAllgrove or AAA (Triple A) syndrome is a rare autosomal recessive disease characterized by achalasia, alacrima, adrenocorticotrophic insufficiency and some neurologic abnormalities. Case reportHere we report two brothers 13 and 15years old, with variable features of the syndrome, with prominent neurological symptoms which started in the first decade and, led to motor paralysis and severe muscle wasting in the elderly brother in the second decade of life. Moderate achalasia developed at 9years in the older brother and showed a slowly progressive course with development of chest pain and dysphagia. Alacrima was not evident before the age of 12years.The neurological symptoms were less severe in the younger brother. He suffered alacrima that started at age of 11years and mild dysphagia due to achalasia at age of 12years, both being slowly progressive.This paper highlights early features of this syndrome among Egyptian population and the importance to exclude Allgrove syndrome in the presence of progressive neurological dysfunction. To concludeAllgrove syndrome should be suspected in patients with neurological impairment associated with any of the main symptoms of the syndrome (alacrima, achalasia and adrenal insufficiency).

The relationship between lactate production in the myocardium and the development of chest pain in patients with coronary artery disease (CAD)

Silent myocardial ischemia (SMI) was recognized as early as the beginning of the 20th century. The consequences of silent ischemia can be grave because lack of symptoms and lack of symptom recognition. Early detection of SMI may prevent many episodes of sudden cardiac death annually. However, the role and behavior of the factors determining the occurrence of silent myocardial ischemia have not been fully established. To detect if there is a relationship between the level of lactate production in the myocardium and the development of chest pain in patients with coronary artery disease (CAD). This study was carried out in cardiology and biochemistry departments, Zagazig University on 46 patients (38 males) with coronary artery significant disease (>70% stenosis) including left anterior descending artery disease. Cannulation of coronary sinus with Amplatz left catheter was done and a pigtail catheter was introduced into the mid LV cavity. Right atrial pacing was done and the heart rate was increased stepwise 10 bpm/1 min until a maximum of 150 bpm or chest pain occurs or significant S–T segment depression occurs. LV gram for assessment of systolic function and blood samples were withdrawn from the LV and coronary sinus before and after pacing induced ischemia and the patients were classified into two groups according to development of chest pain (angina group; 28 patients) during pacing induced tachycardia or not (silent group; 18 patients). 24-h Holter ECG monitoring was done to all patients. Myocardial lactate production was significantly very high in angina group than in silent ischemia group; 10 patients (35.7%) had lactate diminished extraction and 18 patients (64.3%) had lactate production in response to pacing induced tachycardia in group 1 (angina group). All 18 patients (100%) in group 2 (silent ischemia group) had lactate diminished extraction in response to pacing induced tachycardia (<0.001). LV systolic function reduction in response to pacing induced ischemia was non significant between the 2 groups. Silent ischemic attacks represented >80% of total ischemic episodes during 24 h Holter ECG study and it occurred at lower heart rate than angina attacks ( P = 0.03). The magnitude of S–T segment depression was non significant between the two groups. In patients with coronary artery disease, myocardial lactate production is significantly higher in patients with angina than in patients with silent ischemia and as lactate is known (with other metabolic agents) to cause chest pain and this is considered an explanation (mechanism) for the occurrence of silent myocardial ischemia.

Incarcerated Diaphragmatic Hernia With Intrathoracic Bowel Obstruction After Right Liver Donation

Liver transplantation has become an acceptable surgical procedure with the advancement of the technical and rejection considerations involved. Initially nonliving donors were used for transplantation procedures. However, with improved techniques, living donor procedures have become much more frequent. With this, complications involving the transplant organ donor may occur. We present 2 patients with intrathoracic bowel obstruction due to herniation of the small intestine and colon through a defect in the dome of the diaphragm with development of chest pain and gastrointestinal symptoms. Both patients were diagnosed by computerized tomography scan and had a right thoracotomy with lysis of the adhesions, reduction of the hernia, repair of the diaphragm, and mesh reinforcement of the diaphragm. Neither patient had a prior diaphragm defect. These patients, on review of the literature, represent the first 2 such reported cases and suggest the need to be aware of any potential diaphragm defects before closure of the abdomen after resection of the donor liver or if they develop appropriate symptomatology.

Chest Pain During Upper Endoscopy

A 75-year-old male patient visited Seoul St. Mary's Hospital for regular check-up after endoscopic resection of the early gastric cancer. He complained of mild and intermittent dysphagia to solids and liquids for 1 year duration. Frequency of dysphagia increased recently. Previously performed upper endoscopies were reported as normal. After insertion of endoscopy, he complained of severe chest pain. The esophageal mucosa appeared normal but there were severe contractions leading to resistance in advancing the scope in the mid esophagus (Fig. 1). Esophagogram showed a corkscrew appearance on the mid and lower part of the esophagus (Fig. 2). Esophageal manometry disclosed the hypercontractile amplitudes of 365 mmHg (Fig. 3). A normal relaxation of the lower esophageal sphincter ruled out achalasia. Cardiac evaluation revealed nonspecific findings. These findings led to the diagnosis of diffuse esophageal spasm (DES), which was responsible for the chest pain. Chest pain subsided with the treatment of proton pump inhibitor, verapamil and isosorbide mononitrate. Figure 1 Upper endoscopy before (A) and after (B) the development of chest pain. Powerful contraction of mid esophagus is observed in the figure 1B. Figure 2 Corkscrew esophagus on barium esophagogram. Figure 3 Esophageal manometry shows multiple spontaneous simultaneous contractions. The amplitudes of these contractions are particularly high. The pain associated with DES are very variable in severity and sometimes can mimic that of angina pectoris.1 Upper endoscopy is firstly recommended to detect structural causes of dysphagia and noncardiac chest pain. In most affected patients, the esophagus retains the ability to propagate normal peristaltic contractions. As endoscopy has substantial limitations in assessing abnormal esophageal motility in DES, the intraluminal manometry is usually needed for the diagnosis of increased pressure of nonperistaltic contractions.2 The presented case showed interestingly endoscopic findings strongly suggestive of DES along with compatible radiographic and manometric findings.

The Use of Simulation to Assess Dynamic Decision Making.

INTRODUCTION: In dynamic situations such as in the intensive care unit, decisions are often made by applying precompiled rules for a particular event relying on past experience to predict future outcomes. Klein has described this type of thinking as recognition primed decision-making 1. Two common clinical conditions in critically ill patients include hypotension from sepsis and chest pain from myocardial ischemia. If presented with a patient with either one of these conditions, a precompiled response could be used to start treatment. Treatment challenges arise if clinicians are presented with a patient with both problems. We retrospectively reviewed the treatment of a simulated septic patient who subsequently developed myocardial ischemia. MATERIALS AND METHODS: Following IRB approval, we reviewed ten audiovisual recordings of fully immersive high fidelity ICU course simulations taught at the Palo Alto VA from June 2003-June 2004. Medical management was first provided by an intern with a senior resident arriving, on average 12 minutes, into the scenario. The METI-HPS was used for all of the simulations. The scenario involved an elderly male admitted to the ICU for low urinary output, increasing heart rate and hypotension, with the presumptive diagnosis of urosepsis. The patient developed chest pain and ischemic EKG changes 8 minutes into the scenario. The teams’ overall performance was scored as either management of primary sepsis, primary ischemia, or both. RESULTS: All ten teams began the appropriate treatment of sepsis (additional intravenous access and fluid). Upon the development of chest pain (HR 120’s BP 80’s/50’s) 5 teams deviated from the sepsis treatment plan and converted to a primary cardiac treatment plan, including giving aspirin, nitrates, heparin and morphine. Four teams continued with the sepsis pathway, including either starting or escalating vasopressors, and one team treated the patient as having both a cardiac and a septic event. DISCUSSION: Medical decision-making often relies on pattern recognition. Using precompiled responses, for example treatment pathways, cognitive aids, and mnemonics; a physician can make decisions more efficiently. If faced with novel situations or if conflicting treatment goals arise, physicians are required to use abstract reasoning to determine the most appropriate next step. In this scenario, the patient developed myocardial ischemia secondary to increased demand from the hypotension and tachycardia caused by sepsis. Half the teams converted to a primary cardiac pathway treating the patient’s ischemia as a primary cardiac event. This conversion not only delayed appropriate treatment but also resulted in morbidity. Cognitive tunneling may have occurred as the teams relied on familiar medical management even when it was inappropriate. We could not question the participants on why they chose a primary cardiac treatment pathway, as this was a retrospective study. Further investigation is needed to determine if these errors were secondary to lack of experience or represent a more fundamental flaw in the way dynamic decision-making is taught in medical education. Simulation is a useful method to probe such issues.

The “Good Cholesterol”

Atherosclerosis is an insidious and dangerous disease: a progressive chemical and structural injury to the blood vessels in such critical organs as the heart, brain, and kidney. The hallmark feature of atherosclerosis is the buildup of cholesterol into lesions called plaques that can reduce the flow of blood. When the delivery of blood to heart muscle drops enough, this can result in the development of chest pain or angina. Angina indicates that the heart muscle is not receiving enough oxygen to carry out its pumping functions. Atherosclerotic plaques can also suddenly rupture, develop a blood clot on their surface, and completely choke off a portion of heart muscle. This chain of events frequently results in heart attack or sudden death without warning. Atherosclerotic disease also predisposes people to stroke, peripheral vascular disease, lower-extremity amputation, and loss of kidney function, among other devastating outcomes. Despite all that we have learned in the past 50 years, atherosclerosis remains the No. 1 killer of men and women and the chief reason for loss of quality of life in Western countries. We are, however, gaining ground. Considerable research has revealed the importance of factors that increase an individual’s risk for developing this disease. Among the most important of these risk factors are elevated blood pressure, diabetes mellitus, obesity, inactivity, smoking, and cholesterol levels. When your physician measures your cholesterol level, he or she is looking at your lipid profile, which comprises low-density lipoprotein cholesterol (LDL-C, or the “bad” cholesterol), triglycerides (blood fats), and high-density lipoprotein cholesterol (HDL-C, or the “good” cholesterol). In a general way, when it comes to measurement of your LDL-C and triglyceride values, a lower value is better because these lipids drive the development and progression of atherosclerosis. In sharp contrast, when it …

Different long-term course between chest pain and exercise-induced ST depression in syndrome X.

The aim of the present study was to assess the long-term clinical course of patients with syndrome X, focusing on different courses between exercise-induced ST depression and chest pain. Forty-three patients with syndrome X were followed up for 6.4 +/- 3.8 years. They were divided into the 3 groups according to chest pain: disappeared (n = 24), improved (n = 14), or unchanged (n = 5). No patients had cardiac events and all had a favorable long-term prognosis. In patients showing disappearance of chest pain, exercise-induced ST depression and rate-pressure product (RPP) at peak exercise did not change during follow-up. However, ST depression and RPP decreased significantly in those with improved chest pain. These observations suggest that abnormal pain perception plays an important role in the development of chest pain.

Relation between the electrocardiographic stress test and degree and location of myocardial ischemia

Factors that influence frequency and location of stress-induced electrocardiographic (ECG) ST depression and the development of chest pain are incompletely understood. We studied 331 patients with ischemic myocardial nuclear defects in response to routine clinical treadmill testing with simultaneous ECG recording. Nuclear defects were analyzed for location and extent of myocardium involved. Exercise-induced ischemic ST changes were demonstrated in 59% of patients (196 of 331). Subjects with stress-induced ECG changes and/or chest pain had more extensive nuclear perfusion defects. Diabetic patients were significantly less likely to experience chest pain (24%) versus nondiabetics (41%) during testing (p = 0.04). Larger perfusion defects were associated with greater magnitude, lead distribution, and incidence of ECG changes. The number of ECG lead zones (anterior, lateral, and inferior) responding positively were related to both magnitude of ST depression and severity of ischemia, but not to location of ischemic defects. Regardless of location of ischemia, ST depression occurred with similar frequency. Thus, exercise-induced ECG ST depression remains a valuable indicator of the severity of myocardial ischemia. Greater ST depression involving multiple leads usually signified extensive myocardial ischemia, but provided no information regarding its location. Anginal-type chest pain induced by exercise testing also denoted more extensive ischemia.

Chest pain after coronary interventional procedures. Incidence and pathophysiology.

Chest pain following successful percutaneous coronary interventions is a common problem. Although the development of chest pain after coronary interventions may be of benign character, it is disturbing to patients, relatives and hospital staff. Such pain may be indicative of acute coronary artery closure, coronary artery spasm or myocardial infarction, but may also simply reflect local coronary artery trauma. The distinction between these causes of chest pain is crucial in selecting optimal care. Management of these patients may involve repeat coronary angiography and additional intervention. Commonly, repeat coronary angiography following percutaneous transluminal coronary angioplasty (PTCA) in patients with chest pain demonstrates widely patent lesion sites suggesting that the pain was due to coronary artery spasm, coronary arterial wall stretching or was of non-cardiac origin. As reported by the National Heart, Lung and Blood Institute PTCA Registry, 4.6% of patients after angioplasty have coronary occlusions, 4.8% suffer a myocardial infarction, and 4.2% have coronary spasm. The frequency of chest pain after new device coronary interventions (atherectomy and stenting) seems to be even higher. However, only the minority of patients with post-procedural chest pain have indeed an ischemic event. Therefore, the vast majority of patients have recurrent chest pain without any signs of ischemia. There is some evidence that non-ischemic chest pain after coronary interventions is more common after stent implantation as compared to PTCA (41% vs. 12%). This may be due to the continuous stretching of the arterial wall by the stent as the elastic recoil occurring after PTCA is minimized. In conclusion, chest pain after coronary interventional procedures may potentially be hazardous when due to myocardial ischemia. However, especially after coronary stent placement, cardiologists must consider "stretch pain" due to the overdilation and stretching of the artery caused by the stent in the differential diagnosis. Clinically, it is, therefore, important to recognize that in addition to ischemia-related chest pain other types of chest pain do exist with cardiac origin.

Changes in coronary sinus pH during dipyridamole stress in patients with hypertrophic cardiomyopathy.

The presence of angina pectoris and myocardial scarring in patients with hypertrophic cardiomyopathy (HCM) suggests that myocardial ischemia is a factor in the pathophysiology of the disease. The clinical evaluation of ischaemia is problematic in HCM as baseline electrocardiographic abnormalities are frequent and thallium-201 perfusion abnormalities correlate poorly with anginal symptoms. Coronary sinus pH measurement using a catheter mounted pH electrode is a validated sensitive technique for the detection of myocardial ischaemia. 11 patients with HCM and chest pain (eight men; mean (SD) (range) age 36 (11) (19-53) years) and six controls (two men; mean (SD) (range) age 49 (11) (31-62) years) with atypical pain and normal coronary angiograms were studied. Eight patients with HCM had baseline ST segment depression of > or = 1 mm and four had reversible perfusion defects during stress 201TI scintigraphy. A catheter mounted hydrogen ion sensitive electrode was introduced into the coronary sinus and pH monitored continuously during dipyridamole infusion (0.56 mg/kg over four min). The maximal change in coronary sinus pH during dipyridamole stress was greater in patients with HCM than in controls (0.082 (0.083) (0 to -0.275) v 0.005 (0.006) (0 to -0.012), P = 0.02). In six patients (four men; mean (SD) (range) age 29 (9) (19-40 years) the development of chest pain was associated with a gradual decline in coronary sinus pH (mean 0.123 (0.089)), peaking at 442 (106) s. There were no relations among left ventricular dimensions, maximal wall thickness, and maximum pH change. In patients with HCM there was a correlation between maximum pH change and maximum heart rate during dipyridamole infusion (r = 0.70, P = 0.02). This study provides further evidence that chest pain in patients with HCM is caused by myocardial ischaemia. The role of myocardial ischaemia in the pathophysiology of the disease remains to be determined but coronary sinus pH monitoring provides a method for quantifying and prospectively assessing its effects on clinical presentation and prognosis.

Buccal versus intravenous nitroglyerin in unstable angina pectoris

The clinical syndrome of unstable angina includes patients with the first onset of angina, change in a previous stable pattern or the development of chest pain at rest. Administration of intravenous nitroglycerin is established therapy in unstable angina. Buccal nitroglycerin has been introduced as an alternative means of administering nitroglycerin, which provides relief of anginal pain within 2 to 3 min and a sustained effect for 3 to 5 h. Twenty-nine patients admitted to the coronary care unit due to unstable angina were randomized to receive treatment with nitroglycerin i.v. for 24 h or buccal nitroglycerin every 4 h. Therapy was titrated according to haemodynamic effects. The mean dose of buccal nitroglycerin was 4.42 mg versus 0.45 micrograms.kg-1.min-1 in the intravenous group. The efficacy of treatment was similar in the two groups. Buccal nitroglycerin appeared to cause fewer adverse effects, especially less haemodynamic intolerance and headache, although the differences were not significant. Repeated administration of buccal nitroglycerin appears to be a safe and well tolerated alternative to high-dose i.v. nitroglycerin treatment in unstable angina pectoris.

HISTAMINE‐INDUCED CORONARY ARTERY SPASM: THE CONCEPT OF ALLERGIC ANGINA

SUMMARYHistamine, the main amine released during allergic reactions, can provoke coronary arterial spasm manifested as angina pectoris. This has been shown during clinical and laboratory studies. The effects of histamine on cardiac function are mediated via H1‐ and H2‐ receptors situated on the four cardiac chambers and coronary arteries. Coronary arteries of cardiac patients are hyperactive and contain stores of histamine which can initiate coronary artery spasm.Clinical observations indicate that angina pectoris or acute myocardial infarction can be provoked by acute allergic reaction. The coincidental occurrence of chest pain and allergic reaction accompanied by clinical and laboratory findings of classical angina pectoris seems to constitute the syndrome of allergic angina. The clinical symptoms of allergic angina include chest discomfort, dyspnoea, faintness, nausea, pruritus and urticaria. They are accompanied by signs such as hypotension, diaphoresis, pallor and bradycardia. There are also electrocardiographic findings indicating myocardial ischaemia, arrhythmias and conduction defects.Thus, in patients undergoing acute allergic reaction, the development of chest pain could be explained by the mechanism of coronary arterial spasm provoked by the release of histamine, which constitutes the syndrome of allergic angina.

Effect of Transient Myocardial Ischemia on the Transmitral Blood Flow Profile

To evaluate the effect of transient myocardial ischemia on the transmitral blood flow profile, pulsed Doppler echocardiography was performed in 10 anesthetized dogs during brief occlusion of the coronary artery and in 79 patients with coronary artery disease (CAD) and 19 control subjects who underwent esophageal pacing or dipyridamole stress tests. During coronary artery occlusion, the peak velocity of the rapid filling wave (R) was rapidly reduced and that of atrial contraction (A) augmented. These changes of overall left ventricular diastolic filling variables surprisingly coincided with rapid deterioration of systolic wall thickening at the ischemic segment. In the clinical study, the transmitral flow profile did not change in controls during esophageal pacing. We observed similar changes in the transmitral flow profile in the experimental study in CAD patients. The deceleration time of the early diastolic filling wave was not changed in controls, but was significantly prolonged in CAD patients. Preadministration of sublingual nitroglycerin normalized the postpacing responses of peak velocities and deceleration times induced in CAD patients. With intravenous administration of 0.56 mg/kg of dipyridamole R and A increased, but the A/R ratio was unchanged in both controls and CAD patients. The deceleration halftime, however, was prolonged in CAD patients, as shown during esophageal pacing. These changes of transmitral flow patterns were transient and recovered within a few minutes. Furthermore, they were noted more frequently than the development of chest pain or electrocardiographic ST depression. However, induced changes of transmitral flow profile were not significantly different between patients with multivessel disease and those with single-vessel disease in both stress tests, so that there were limitations in diagnosing the extent of coronary artery disease. These findings suggest that peak velocities or deceleration time responses in transmitral blood flow are early and sensitive markers for evaluating abnormal left ventricular diastolic filling during transient myocardial ischemia. This noninvasive technique may be a reasonable alternative to other imaging examinations for detection and functional assessment of patients with CAD.

Use of nitrates in the treatment of unstable and variant angina.

Unstable angina is a clinical syndrome that includes patients with new onset of angina, a change in a previous stable pattern, or the development of chest pain at rest. Generally, more than 90% of patients with this syndrome have significant fixed atherosclerotic coronary artery disease. Other complex, interacting pathophysiological mechanisms may include coronary vasoconstriction, plaque rupture and thrombosis. Therapeutic strategies aim at either reduction of myocardial oxygen demand or restoration of coronary blood flow. Both alternatives have been suggested as treatment of choice. However, as long as the pathophysiological mechanism(s) is unknown in the individual case, the treatment will mainly be empirical or based on results from clinical trials of heterogeneous groups of patients with unstable angina with probably varying aetiology. The results from such studies indicate that some strategies may be of value, but others may even be harmful in treatment of patients with this unstable syndrome. In this situation nitrates seem to be a safe drug which may be used in most forms of irrespective of the underlying pathophysiological mechanism(s).