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Histamine-induced coronary artery spasm: The concept of allergic angina
Abstract
Histamine, 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 H ¹ ‐ and H 2 ‐ 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.
... Kounis syndrome (KS) is a condition characterized by an allergic reaction leading to an acute coronary syndrome. It was initially identified and reported by Kounis and Zavras in 1991 and is alternatively referred to as "allergic angina syndrome" or "allergic myocardial infarction" [1]. ...
... Kounis syndrome (KS) is a condition characterized by an allergic reaction leading to an acute coronary syndrome. It was initially identified and reported by Kounis and Zavras in 1991 and is alternatively referred to as "allergic angina syndrome" or "allergic myocardial infarction" [1]. ...
... The association of cardiovascular manifestations and hypersensitivity reactions has been well-established since 1991 when the first case of KS was reported as MI or coronary vasospasm could be triggered by a severe allergic reaction in the setting of mast cell degranulation and histamine release [5]. Due to severe morbidity and mortality, KS requires urgent evaluation and appropriate management. ...
... Kounis syndrome, initially described in 1991, refers to allergic angina resulting from histamine-induced coronary spasm during an acute allergic reaction. 1 Subsequently, in 2016, its definition expanded to include the simultaneous occurrence of acute coronary syndrome (ACS) with mast cell and platelet activation due to an allergic or anaphylactic reaction. 2 This syndrome is categorized into three variants, with type I involving ACS associated with coronary spasm. ...
Background
Type I variant Kounis syndrome is characterized by coronary spasm following an allergic or anaphylactic reaction. Coronary spasm is also recognized as a contributing factor in spontaneous coronary artery dissection (SCAD).
Case summary
A 46-year-old woman presented to the emergency room with a chief complaint of chest discomfort following the ingestion of a steamed bun. A marked decrease in systolic blood pressure and a prominent rash on her forearms and groin suggested anaphylactic shock. Upon stabilization of vital signs, acute coronary syndrome (ACS) was suspected based on electrocardiogram findings and symptoms, prompting an emergency coronary angiography (CAG). The CAG revealed severe stenosis with coronary artery dissection in the right coronary artery, and a stent implantation was performed. Given the suspicion of type I variant Kounis syndrome, a spasm provocation test was performed, yielding a positive result. Six years later, she experienced chest discomfort while sleeping and was admitted to our emergency department. An electrocardiogram showed ST-segment elevation in leads II, III, and aVF. An emergency CAG identified a severely stenotic lesion with coronary artery dissection in the right coronary artery, leading to a diagnosis of SCAD. Direct stenting was performed at the stenotic site. The patient was discharged following intensification of medication.
Discussion
This report describes a rare case of a middle-aged woman with two episodes of ACS caused by both allergic and nonallergic coronary artery dissection. These episodes suggest that a shared underlying coronary vasospasm in both conditions may be a common trigger for coronary artery dissection.
... Mast cell granules contain various mediators, particularly heparin and histamine, and also tryptase, chymase, carboxypeptidase, cathepsin C and G (5). KS is an acute coronary syndrome characterized by coronary artery spasm caused by these inflammatory mediators released into the environment as a result of endothelial dysfunction or mast cell degranulation with microvascular manifestation. This allergic angina syndrome caused by allergic reactions was first described in 1991 (6). Most cases (80%) occur within 1 h of exposure to the trigger. ...
... Among the spectrum of allergic reactions, Kounis syndrome (KS) is defined as an acute coronary syndrome related to the release of allergic inflammatory mediators which can affect the coronary arteries [5]. It is considered a complex multisystem disease including Diagnostics 2024, 14, 1092 2 of 8 any coronary syndrome related to mast-cell-associated disorders and inflammatory cell interactions [6]. ...
Kounis Syndrome (KS) is a clinical entity triggered by allergic or hypersensitivity reactions capable of inducing acute coronary events. Several causes can induce KS, including drugs and insect stings. Here, a rare case of post mortem assessment of fatal KS related to fluorescein retinal angiography has been reported. An 80-year-old man in follow-up for a retinal vein thrombosis underwent a retinal fluoroangiography. Approximately 30 min later, the patient complained of sweating and dizziness, and suddenly lost consciousness due to a cardiac arrest. Despite the immediate cardiopulmonary resuscitation, he died. The autopsy revealed foamy yellowish edema in the respiratory tract and coronary atherosclerosis with eccentric plaques partially obstructing the lumen. The routine histology highlighted lung emphysema and myocyte break-up with foci of contraction band necrosis at the myocardial tissue. Biochemistry showed increased serum tryptase, troponin, and p-BNP. Activated and degranulated (tryptase) mast cells were detected, using immunohistochemistry, in the larynx, lungs, spleen, and heart. Acute myocardial ischemia due to allergic coronary vasospasm related to fluorescein hypersensitivity has been assessed as cause of death. KS-related deaths are considered rare events, and the post mortem assessment of KS quite difficult. The integration of several investigations (gross and microscopic examination, biochemistry, immunohistochemistry) can provide useful findings to support the diagnosis, helping to reduce the unrecognized cases as much as possible.
... The clinical symptoms of Kounis syndrome include chest discomfort, dyspnoea, faintness, nausea, pruritus, and urticaria, and they are accompanied by signs such as hypotension, diaphoresis, pallor, and bradycardia. There are also ECG findings indicating myocardial ischemia, arrhythmias, and conduction defects [2]. This syndrome has been reported in conjunction with bee stings, antibiotics, and other causes [3][4][5]. ...
... Kounis syndrome, first described by Kounis and Zavras in 1991, represents a unique clinical entity that bridges the fields of allergy and cardiology. It is characterized by the development of acute coronary syndromes, including angina, myocardial infarction, or sudden cardiac death, in the setting of allergic or hypersensitivity reactions. ...
Kounis syndrome, also known as allergic angina or allergic myocardial infarction, is a rare but potentially life-threatening condition characterized by the acute onset of chest pain, myocardial infarction, or sudden cardiac death in the setting of allergic or hypersensitivity reactions. The syndrome encompasses a spectrum of acute coronary syndromes triggered by various allergic insults, including medications, insect stings, food allergens, and environmental exposures. The pathophysiology involves the activation of mast cells and platelets, leading to coronary artery spasm, atheromatous plaque erosion or rupture, and subsequent myocardial ischemia or infarction. Diagnosis can be challenging due to the diverse clinical presentations and the need for a high index of suspicion. Management includes the identification and avoidance of triggers, along with the use of standard therapies for acute coronary syndromes. This review aims to provide a comprehensive overview of Kounis syndrome, focusing on its pathophysiology, clinical manifestations, diagnostic considerations, and therapeutic strategies.
... Pfister and Plice reported the first case of acute MI linked to urticaria brought on by penicillin therapy in 1950. 20 Kounis and Zavras did not coin the term "allergic angina syndrome" until 1991, as coronary spasm evolved into allergy acute MI. 21 Kounis syndrome (KS) is defined as the concurrence of acute coronary syndromes like coronary spasm (type I variant), acute myocardial infarction (type II), and stent thrombosis (type III) in the setting of allergic or hypersensitive reactions, anaphylactic or anaphylactoid insults, and conditions associated with mast cell and platelet activation involving connected and interacting inflammatory cells. 22,23 Histamine, which is generated when mast cells degranulate, is typically linked to severe allergy and anaphylactic reactions, but it can also occasionally cause atheromatous plaque erosion with rupture or severe coronary artery spasm. ...
Despite the noteworthy advancements and the introduction of new technologies in diagnostic tools for cardiovascular disorders, the electrocardiogram (ECG) remains a reliable, easily accessible, and affordable tool to use. In addition to its crucial role in cardiac emergencies, ECG can be considered a very useful ancillary tool for the diagnosis of many non-cardiac diseases as well. In this narrative review, we aimed to explore the potential contributions of ECG for the diagnosis of non-cardiac diseases such as stroke, migraine, pancreatitis, Kounis syndrome, hypothermia, esophageal disorders, pulmonary embolism, pulmonary diseases, electrolyte disturbances, anemia, coronavirus disease 2019, different intoxications and pregnancy.
Background: Kounis syndrome is defined as the occurrence of acute coronary artery syndrome as a result of activation of inflammatory cells after conditions such as allergy, hypersensitivity, anaphylaxis or anaphylactic reactions. This case reports were presented to provide the latest knowledge on Kounis syndrome, increase awareness of this disease among healthcare providers and researchers, and promote early and appropriate diagnosis and management of this syndrome. Summary of Cases: In the first case, a 45-year-old female patient with no history of coronary artery disease developed anaphylaxis due to a locally applied anesthetic drug. This led to transient coronary artery vasospasm and acute coronary syndrome. In the second case, a 70-year-old male patient with a history of coronary artery disease developed anaphylaxis due to a bee sting. This caused rupture of the coronary artery plaque, resulting in inferior myocardial infarction. In the third case, a 73-year-old male patient with a stent in his coronary artery developed an allergic reaction/anaphylaxis to midazolam, which was administered for sedation before the biopsy procedure. This reaction resulted in restenosis of the old stent and caused an anterior myocardial infarction. Conclusion: Kounis syndrome is a life-threatening condition that requires attention. Ensuring coronary artery patency in the treatment of ischaemia is important to protect cardiomyocyte health and prevent arrhythmias. Ischaemia caused by allergens can be resolved with a combination of antiallergenic treatments. Therefore, for effective management of suspected cases of Kounis syndrome, collaboration between cardiology and allergy-immunology clinics is essential.
Cimetidine is a non-thiourea analogue of metiamide. It is a specific competitive histamine H2-receptor antagonist and is an effective inhibitor of gastric secretion in animals and man with similar pharmacological properties to metiamide. No renal damage or haematological changes were observed in 90-day studies in rats or dogs.
Three patients with cardiomegaly, congestive cardiac failure and blood eosinophilia are described. Necropsy in two disclosed severe mural endocardial fibrosis with superimposed fibrin-platelet thrombi, myocardial scarring, eosinophilic hyperplasia of the bone marrow and spleen without abnormal or leukemic myeloblasts, and occasionally thrombosed small arteries in the heart, spleen, kidneys and lungs. These features are similar to those described in patients with Löffler's fibroplastic parietal endocarditis and in “eosinophilic leukemia” without abnormal myelopoiesis. It is suggested that these two conditions are the same disease. It is also suggested that the predominantly African condition, endomyocardial fibrosis without eosinophilia, may be a late or inactive stage of either Löffler's endocarditis or of “eosinophilic leukemia” without abnormal myelopoiesis.
Because previous reports have suggested that IgE-mediated events may lead to both platelet activation and arterial spasm, a population-based study of 262 men and 315 women, aged 38 to 82, was conducted to investigate the association of serum IgE levels with myocardial infarction, stroke, and noninvasively diagnosed large-vessel peripheral arterial disease. In men with previous myocardial infarction, previous stroke, or current large-vessel peripheral arterial disease, geometric mean serum IgE levels were increased 119 percent, 164 percent, and 78 percent, respectively. These associations were statistically significant (p <0.05). Because IgE was positively or inversely correlated with several traditional cardiovascular disease risk factors, logistic regression was used to evaluate the independent association of IgE with any cardiovascular disease (myocardial infarction, stroke, or large-vessel peripheral arterial disease). In a model including age, cigarette smoking, fasting plasma glucose level, diastolic blood pressure, and low-density lipoprotein cholesterol level as covariates, IgE was positively and independently associated with any cardiovascular disease (p = 0.03). Similar evaluations in women revealed no correlation between IgE and cardiovascular disease by either univariate or multivariable analysis. These data indicate that IgE may be an independent marker for cardiovascular disease in men, and thus suggest IgE-mediated events may play a role in the pathogenesis of cardiovascular disease.
Current information on the role of immune mechanisms in rheumatic fever, postcardiotomy and postinfarction syndromes, cardiomyopathies and other cardiac disorders is reviewed. The possible role of autoimmunity is emphasized in view of the evidence that serum autoantibodies to diverse constituents of heart tissue frequently may be detected in these cardiac disorders.
Several closely related disease entities make up the idiopathic hypereosinophilic syndrome (HES). The syndrome is manifest by persistent and prolonged eosinophilia with organ damage. A group of 14 patients had hematologic, cardiac, and neurologic abnormalities attributable to this disease. Patient survival and response to chemotherapy was significantly better in this group than in previously reported patients. The etiology of HES remains unknown, as does the mechanism of tissue damage.