scholarly journals Coronary spasm secondary to cefuroxime injection, complicated with cardiogenic shock – a manifestation of Kounis syndrome: case report and literature review

2017 ◽  
Vol 7 (7) ◽  
pp. 624-630 ◽  
Author(s):  
Andreas Mitsis ◽  
Evi Christodoulou ◽  
Panayiota Georgiou

Kounis syndrome is defined as the coincidental occurrence of an acute coronary syndrome with hypersensitivity reactions following an allergic event. The three reported variants of Kounis syndrome are vasospastic allergic angina, allergic myocardial infarction and stent thrombosis with occluding thrombus. The syndrome is caused by various inflammatory mediators. The pathophysiological characteristics of Kounis syndrome involve coronary artery spasm and/or atheromatous plaque erosion or rupture during an allergic reaction. Several causes have been described to induce Kounis syndrome, and their number is increasing rapidly. The haemodynamic effect of the syndrome complicated by cardiogenic shock seems to combine allergic shock with extensive peripheral vasodilation and myocardial suppression with the characteristics of cardiogenic shock. Treatment of Kounis syndrome is challenging because it needs management of both cardiac and allergic manifestation simultaneously. We present a case report of type I Kounis syndrome, with coronary spasm secondary to cefuroxime injection complicated with cardiogenic shock. A brief review of the literature on the various facets of this condition is also provided.

2016 ◽  
Vol 223 ◽  
pp. 959-961 ◽  
Author(s):  
Hyung Il Kim ◽  
Kyoung Chul Cha ◽  
Yong Sung Cha ◽  
Oh Hyun Kim ◽  
Hyun Kim ◽  
...  

2019 ◽  
Vol 72 (1) ◽  
pp. 137-141
Author(s):  
Olga Wajtryt ◽  
Tadeusz M Zielonka ◽  
Aleksandra Kaszyńska ◽  
Andrzej Falkowski ◽  
Katarzyna Życińska

Kounis syndrome or allergic myocardial infarction is an acute coronary syndrome in the course of an allergic reaction. In allergic patients in response to a specific condition - nourishment, inhalation, environmental substances, drug or insect bite there is an allergic reaction involving many different cells and mediators that can cause coronary artery spasm or initiate the process of rupture and activation of atherosclerotic plaque resulting in acute coronary syndrome. The paper describes a case of a young man with allergy to pollen and confirmed sensitization to nuts, who developed a full-blown anaphylactic shock after eating the nut mix and experienced a rapidly passing acute coronary syndrome with troponin up to 4.7 μg/L. An increased concentration of tryptase (15 μg/L), total IgE (> 3,000 IU/mL) and specific anti-nut IgE (55.1 kUA/L) were found. Based on the course of the disease and the results of allergic and cardiac tests, allergic type 1 myocardial infarction, i.e. caused by coronary artery spasm, was diagnosed. During the hospitalization, the patient’s condition improved quickly and after a few days he left the hospital without the signs of permanent damage to the heart muscle.


2019 ◽  
Vol 12 (12) ◽  
pp. e232472
Author(s):  
Luca Conti ◽  
Kelly Gatt ◽  
Christopher Zammit ◽  
Karen Cassar

Acute coronary syndrome occurring during the course of a type I hypersensitivity reaction constitutes Kounis syndrome. We report a case of a 64-year-old man who presented with a non-ST elevation myocardial infarction and peripheral blood eosinophilia. He had rhinitis and constitutional symptoms for several days prior to presentation. Blood investigations revealed moderate eosinophilia and elevated IgE levels. A cardiac MRI showed generalised oedema with a subtle wall motion abnormality in basal inferior/inferolateral wall, and subendocardial high signal on late gadolinium enhancement suggesting a localised myocardial infarction. A coronary angiogram then revealed triple vessel disease. A diagnosis of Kounis syndrome was made. Within days of starting appropriate treatment, the patient’s eosinophil count returned to normal with improvement of clinical picture.


2020 ◽  
Vol 75 (11) ◽  
pp. 3203
Author(s):  
Mayara Reis Cardoso Ferreira ◽  
Luciano Moreira Baracioli ◽  
Filomena Regina Barbosa Gomes Galas ◽  
Talia Dalcoquio ◽  
Remo Holanda Furtado ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-3
Author(s):  
Sazzli Kasim ◽  
Rafidah AbuBakar ◽  
Eugene McFadden

Myocardial infarction as a result of wasp stings is a rare manifestation of acute coronary syndromes. It has been ascribed to kounis syndrome or allergic angina whose triggers include mast cell degranulation leading to coronary vasospasm and/or local plaque destabilisation. Its exact pathophysiology is still not clearly defined. We present a case of an acute coronary syndrome as a consequence of wasp stings and discuss its possible aetiology.


Vaccines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 38
Author(s):  
Anastasios Roumeliotis ◽  
Periklis Davlouros ◽  
Maria Anastasopoulou ◽  
Grigorios Tsigkas ◽  
Ioanna Koniari ◽  
...  

Kounis syndrome (KS) has been defined as acute coronary syndrome (ACS) in the context of a hypersensitivity reaction. Patients may present with normal coronary arteries (Type I), established coronary artery disease (Type II) or in-stent thrombosis and restenosis (Type III). We searched PubMed until 1 January 2020 for KS case reports. Patients with age <18 years, non-coronary vascular manifestations or without an established diagnosis were excluded. Information regarding patient demographics, medical history, presentation, allergic reaction trigger, angiography, laboratory values and management were extracted from every report. The data were pulled in a combined dataset. From 288 patients with KS, 57.6% had Type I, 24.7% Type II and 6.6% Type III, while 11.1% could not be classified. The mean age was 54.1 years and 70.6% were male. Most presented with a combination of cardiac and allergic symptoms, with medication being the most common trigger. Electrocardiographically, 75.1% had ST segment elevation with only 3.3% demonstrating no abnormalities. Coronary imaging was available in 84.8% of the patients, showing occlusive lesions (32.5%), vascular spasm (16.2%) or normal coronary arteries (51.3%). Revascularization was pursued in 29.4% of the cases. In conclusion, allergic reactions may be complicated by ACS. KS should be considered in the differential diagnosis of myocardial infarction with non-obstructive coronary arteries.


2019 ◽  
Vol 39 (7) ◽  
pp. 641-646
Author(s):  
Yosuke WATANABE ◽  
Kazunori SENBA ◽  
Daishiro HORIUCHI ◽  
Hiroki TOKIWA ◽  
Yoko DESAKI
Keyword(s):  
Type I ◽  

2019 ◽  
Vol 2019 ◽  
pp. 1-3 ◽  
Author(s):  
W. D. D. Priyankara ◽  
E. M. Manoj ◽  
A. Gunapala ◽  
A. G. R. M. A. Ranaweera ◽  
K. S. Vithanage ◽  
...  

Kounis syndrome is associated with mast cell activation resulting in acute coronary syndrome secondary to an allergic insult. Various drugs such as antibiotics, analgesics, and environmental exposures such as bee, wasp sting, and poison ivy are known to induce Kounis syndrome. A 68-year-old man admitted with a cobra bite on both hands to emergency care unit and sustained cardiorespiratory arrest. Electrocardiogram, taken 6 hours after the cardiac arrest, showed ST elevations in leads V2 to V5 suggestive of anterior ST elevation myocardial Infarction (STEMI). Serum Troponin was 10 ng/ml (control= <0.5). Serum IgE levels were significantly high (19155IU/ml, baseline 100). 2-Dimensional echocardiogram showed anterior and apical-septal hypokinesia with left ventricular ejection fraction of 30-35%. Coronary angiogram was normal. He remained hypotensive requiring inotropic and vasopressor support during ICU stay. This was a case of Kounis syndrome leading to cardiogenic shock secondary to Cobra (naja naja) bite. This is the only reported case of cobra bite causing Kounis syndrome and cardiogenic shock. Identification of the cause of myocardial infarction in snake envenomation is useful in the management as some of the drugs like adrenaline, morphine, and beta blockers may worsen the clinical syndrome if it is due to Kounis syndrome.


Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Mian Tanveer Ud Din ◽  
Kushani Gajjar ◽  
Valentyna Ivanova

Kounis syndrome(KS), first described in 1991, is defined as concurrence of acute coronary syndrome and anaphylactic events. Primary mechanism of KS is interaction of mast cells with T-lymphocytes and macrophages via multidirectional stimuli leading to platelets activation. Case presentation: A 35 y.o. tennis coach with multiple sclerosis is admitted to the medical ICU with anaphylaxis after receiving Ocrelizumab infusion. Vital signs on presentation are significant for hypotension with blood pressure of 69/30 mm Hg, sinus tachycardia to 110 bpm and hypoxia with SatO2 88% on room air. Other investigations including chest x-ray, EKG and blood work are unrevealing for secondary pathological process outside of anaphylaxis. She undergoes fluid resuscitation followed by epinephrine drip for persistent hypotension. In addition methylprednisolone, famotidine and diphenhydramine are administered. She requires escalating doses of epinephrine and subsequently develops chest pain with troponin elevation to 0.29 ng/ml and EKG concerning for new ST depression and T wave inversion in II, III, aVF, V2 - V6 leads. Urgent echocardiography revealed normal biventricular function with no wall motion abnormalities and is only significant for moderate MR. Given excellent underlying functional capacity and no underlying cardiac risk factors, she was treated for Kounis syndrome by treating underlying anaphylaxis and weaning epinephrine as able with additional fluid resuscitation. Her chest pain resolved and EKG normalized with eventual discontinuation of epinephrine. Repeat echocardiography revealed preserved left ventricular (LV) function and mild MR. Discussion: KS is not a rare disease but easily overlooked and infrequently diagnosed. Our patient had the type I variant: endothelial dysfunction or microvascular angina in absence of cardiac risk factors. Inflammatory mediators can cause vasospasm and catecholamines used for treatment may potentiate it therefore requiring thoughtful dosing and appropriate duration of treatment. Prompt recognition is crucial for appropriate management of anaphylatic shock followed by that of ACS if LV function declines or risk factors for cardiac disease are present.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G Kawamura ◽  
H Okayama ◽  
S Kido ◽  
T Aono ◽  
K Matsuda ◽  
...  

Abstract Background Substantial cases of out-of-hospital cardiac arrest (OHCA) due to acute coronary syndrome have been recognized thus far, but there have been few reports about the aetiology of patients with OHCA without the organic heart disease. Especially, coronary artery spasm would be one of the causes of OHCA. Purpose This study aimed to investigate causes of OHCA without the organic heart disease and to investigate the characteristics and angiographic findings of OHCA patients with vasospastic angina (VSA). Methods Between January 2010 and April 2018, 920 patients with OHCA caused by probable or definite cardiovascular disease were transferred to our hospital. Return of spontaneous contraction was successfully achieved in 151 patients, among whom diagnosis was made in 130 patients. First, we analysed the causes of OHCA in these patients. Second, we compared clinical and angiographic characteristics between the VSA group with OHCA (OHCA-VSA) and the VSA group without OHCA (stable VSA; n=72) from our database. Results Among the 130 patients, 95 (73%) had the organic heart disease; 72, acute coronary syndrome; 19, myocardial disease; 2, valvular heart disease; and 1, congenital heart disease. There were 35 patients (27%) without the organic heart disease. Nineteen patients had primary (i.e., Brugada syndrome, QT prolongation) or secondary arrhythmia (i.e. drug adverse effect). Electrocardiogram, coronary angiogram, and LV structure and function were normal in 35 patients. However, there were 16 patients (11%) with VSA defined by Japanese guideline. The OHCA-VSA group was significantly younger (50±14) than the stable VSA group (64±11, P=0.003). The incidence of diffuse-type spasm in the OHCA-VSA group (100%) was significantly higher than that in the stable VSA group (100% vs. 69%, P<0.05). In addition, the incidence of triple-vessel coronary spasm in the OHCA-VSA group was significantly higher than that in the stable VSA group (86% vs. 25%, P=0.003). Conclusion OHCA patients without the organic heart disease had considerable cases of VSA, in addition to primary or secondary arrhythmia. Furthermore, the severity of spasm in the OHCA-VSA group was more serious and extensive than in comparison with the stable VSA group.


Sign in / Sign up

Export Citation Format

Share Document