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A 65-year-old woman developed coronary artery vasospasm (CVAS) while being treated with pembrolizumab for stage III melanoma. She experienced chest pain and her troponin levels increased. Invasive coronary angiography showed minor epicardial coronary artery disease, and acetylcholine provocation confirmed the diagnosis of CVAS. The woman was treated with diltiazem and nitroglycerin. It was concluded that her CVAS was caused by pembrolizumab and presented as a myocardial infarction with non-obstructive coronary arteries (MINOCA). [Extracted from the article]

This article presents two case reports of patients with aspirin-exacerbated respiratory disease (AERD) who also experienced lack of efficacy with certain medications. The first case involves a 67-year-old man who developed AERD during treatment with aspirin and exhibited lack of efficacy with benralizumab, verapamil, and isosorbide-mononitrate. The second case involves a 53-year-old man who developed AERD during treatment with aspirin and exhibited lack of efficacy with colchicine and nitroglycerin. Both patients experienced complications related to coronary vasospasm. The article suggests that AERD secondary to aspirin may have been a contributing factor in these cases. [Extracted from the article]

A 61-year-old man experienced a myocardial infarction with non-obstructive coronary arteries (MINOCA) while being treated with olverembatinib for myeloproliferative neoplasm. The patient had a history of well-controlled hypertension and had quit smoking six months prior. He began experiencing chest discomfort and decreased exercise capacity, and a coronary angiography revealed mild stenotic lesions. However, his symptoms worsened, and he developed persistent chest pain. Further testing showed severe stenosis in the left main artery and normal right coronary artery, indicating coronary artery spasm. The patient underwent balloon angioplasty and his symptoms improved. The treatment with olverembatinib was stopped, and he was transferred for additional therapy. It was concluded that the MINOCA was induced by olverembatinib. [Extracted from the article]

A case report in the journal Reactions Weekly describes a 35-year-old woman who experienced a heart attack while being treated with hydroxycarbamide for polycythemia rubra vera. The woman presented with chest pain, nausea, and sweating, and tests revealed elevated levels of cardiac enzymes and abnormal ECG findings. Further investigations showed blockages in her coronary arteries, which were treated with a stent. The heart attack was suspected to be a result of the hydroxycarbamide treatment. The outcome of the patient was not mentioned in the report. [Extracted from the article]

A 68-year-old man experienced coronary vasospasms while undergoing sedative therapy with dexmedetomidine. The patient had persistent atrial fibrillation and was admitted to a hospital in Japan for catheter ablation. After receiving dexmedetomidine, the patient showed ST segment elevation on the ECG, indicating acute myocardial ischemia. Urgent coronary angiography revealed severe narrowing in the right coronary artery, which was resolved with the administration of isosorbide dinitrate. The patient's blood pressure and heart rate returned to normal, and subsequent procedures were completed without further complications. The patient underwent an acetylcholine provocation test to rule out coronary spastic angina, and azelnidipine was resumed. [Extracted from the article]

A case series described three men who developed vasospastic angina (VSA) while being treated with ponatinib or dasatinib for chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia. One of the men also experienced lack of efficacy during treatment with dasatinib and nilotinib for CML. The patients presented with chest pain and were diagnosed with VSA based on symptoms and investigations. Treatment with medications such as diltiazem, isosorbide-dinitrate, benidipine, and rosuvastatin was effective in managing their symptoms. [Extracted from the article]

In a retrospective study of 235 patients, three individuals (two women and one man) between the ages of 44 and 75 developed cardiogenic shock during spasm provocation testing with acetylcholine or ergometrine for the diagnosis of vasospastic angina. The patients received various intracoronary injections, and the diagnosis of vasospastic angina was confirmed in all three cases. Two patients experienced significant coronary vasospasm in the left coronary artery due to acetylcholine, while the remaining patient experienced it due to ergometrine. All patients were successfully treated with isosorbide-dinitrate and norepinephrine. [Extracted from the article]

A 27-year-old woman experienced vasospastic angina after receiving oxytocin for postpartum hemorrhage. She had a medical history of two previous cesarean sections, COVID-19, and oligosymptomatic infection. After receiving oxytocin, she developed symptoms such as headache, palpitations, and chest pain. She was treated with sedation and nitroglycerin to control hypertension. Cardiac ultrasound revealed abnormalities, but her condition improved over time. It was concluded that the vasospastic angina was a result of the oxytocin treatment. [Extracted from the article]

A 27-year-old woman experienced vasospastic angina after receiving oxytocin treatment for postpartum hemorrhage. The woman had a medical history of two previous cesarean sections, COVID-19, and oligosymptomatic infection. After undergoing a cesarean section and receiving oxytocin, she developed symptoms such as headache, palpitations, and chest pain. She was treated with sedation and nitroglycerin to control hypertension. Cardiac ultrasound revealed abnormalities, but her condition improved over time. It was concluded that the woman's vasospastic angina was likely caused by the oxytocin treatment. [Extracted from the article]

A 75-year-old woman developed vasospastic angina with severe left anterior descending (LAD) artery spasm while being treated with carvedilol for stress cardiomyopathy. She initially presented with chest pain and underwent coronary angiography, which revealed stress cardiomyopathy. After being discharged from the hospital, she experienced chest pain and dyspnea and was diagnosed with vasospastic angina with severe LAD spasm based on cardiac magnetic resonance findings. Carvedilol was discontinued, and the woman was treated with other medications for vasospastic angina. Her symptoms improved, and she was scheduled for follow-up at the Women's Heart Clinic. [Extracted from the article]

A 65-year-old man developed coronary vasospasm while undergoing treatment with cisplatin for head and neck squamous cell carcinoma. He experienced chest pain and was admitted to the hospital, where tests revealed transient wall motion abnormalities and ST-elevations. Further examination showed chronic aortic dissection and mild nonobstructive coronary artery disease. The patient was treated with isosorbide mononitrate, and his symptoms resolved. However, he died three days after switching to a different chemotherapy regimen. The cause of death was not specified, and an autopsy was not performed. [Extracted from the article]

A 64-year-old man experienced cardiotoxicity and coronary vasospasm while being treated with capecitabine for pancreatic adenocarcinoma. He presented with chest discomfort during exertion and was diagnosed with capecitabine-associated cardio-toxicity due to coronary vasospasm. He later developed ST segment elevation myocardial infarction. The man was treated with calcium channel blockers and long-acting nitrates, and after four weeks, he was successfully rechallenged with the same chemotherapy regimen without recurrence of symptoms. [Extracted from the article]

A 62-year-old woman experienced a non-ST segment elevation myocardial infarction (NSTEMI) type-I and spontaneous coronary artery dissection (SCAD) while undergoing weight loss therapy with phentermine. She presented to the emergency department with severe chest pain and high blood pressure. The woman had started taking phentermine a few days prior to her admission. After further investigation, it was determined that her NSTEMI and SCAD were likely caused by the phentermine. She was discharged on medication to manage her condition. [Extracted from the article]

A 41-year-old woman experienced coronary vasospasm and polymorphic ventricular tachycardia (PMVT) while undergoing treatment for stage 3 colorectal cancer with fluorouracil, folinic-acid, and oxaliplatin. After her first dose of therapy, she went to the emergency department with chest pain and was diagnosed with myocardial infarction with nonobstructive coronary arteries (MINOCA). Her coronary angiogram was normal, but she was later suspected of having coronary vasospasm. She was treated with IV nitroglycerin and monitored in the critical care unit, but within 24 hours, she developed life-threatening PMVT. Additional medications were administered to prevent further episodes of coronary vasospasm. The development of these conditions was attributed to the FOLFOX regimen. [Extracted from the article]

A 56-year-old man experienced multi-vessel coronary artery vasospasm while being treated with fluorouracil for cecal carcinoma. He was admitted to the hospital with chest discomfort and an electrocardiogram showed elevated ST-segment. Emergency coronary angiography revealed multi-vessel disease related to coronary artery spasms, which was believed to be caused by fluorouracil. The patient was treated with nitroglycerin and the vasospasm resolved. He was discharged after his symptoms completely resolved and his medications were optimized. [Extracted from the article]

A 64-year-old man experienced coronary vasospasm, leading to stress cardiomyopathy, while undergoing treatment with fluorouracil for metastatic oesophageal adenocarcinoma. He presented to the emergency department with chest pain one day after receiving his first dose of chemotherapy. Initial tests showed ST depressions, and further examination revealed angiographically normal coronaries and a ventriculogram consistent with stress cardiomyopathy. The patient's treatment with fluorouracil was discontinued, and he was treated with guideline-directed medical therapy, resulting in the recovery of systolic function. [Extracted from the article]

A 45-year-old man experienced coronary artery spasm while being treated with capecitabine for pancreatic neuroendocrine tumor. He later exhibited lack of efficacy during treatment with lanreotide and temozolomide for the same tumor. The man presented at the emergency room with new exertional chest pain, which improved with rest. He had no history of coronary disease or other cardiac conditions. After discontinuing capecitabine and continuing with temozolomide, his symptoms resolved and he was able to exercise without pain. However, he later experienced disease progression on temozolomide. [Extracted from the article]

Author InformationAn event is serious (based on the ICH definition) when the patient outcome is:• * death * life-threatening * hospitalisation * disability * congenital anomaly * other medically important eventA 65-year-old man developed severe thrombocytopenia during antithrombotic treatment with tirofiban. [Extracted from the article]

Author InformationAn event is serious (based on the ICH definition) when the patient outcome is:• * death * life-threatening * hospitalisation * disability * congenital anomaly * other medically important eventA 22-year-old man (B) developed coronary vasospasm during treatment with testosterone enanthate for muscle gains. [Extracted from the article]

A retrospective review study examined 204 patients with aneurysmal subarachnoid hemorrhage (aSAH) who were treated with heparin for deep vein thrombosis (DVT) prophylaxis. Three patients developed heparin-induced thrombocytopenia (HIT) type II during treatment, and one patient showed lack of efficacy. The patients experienced complications such as vasospasm, delayed cerebral ischemia, and DVT. Treatment with heparin was switched to fondaparinux sodium, and platelet counts recovered within 48 hours after discontinuation of heparin. The study highlights the importance of monitoring patients for HIT and considering alternative treatments when necessary. [Extracted from the article]

A 67-year-old woman experienced coronary vasospasm while being treated with regadenoson for radionuclide myocardial perfusion imaging. She also showed a lack of efficacy with nitroglycerin and nicardipine during treatment for the vasospasm. The woman had a history of hypercholesterolemia, anxiety, and prior breast cancer treatment. After receiving regadenoson, she developed chest pain and ST elevations on an ECG. Further tests revealed severe ischemia and reduced blood flow in her heart. She was treated with nitroglycerin and nicardipine, but continued to experience chest pain and ST elevations. Eventually, her vasospasm resolved and she was discharged with medication to prevent future episodes. [Extracted from the article]

After maintaining 100 g/min dose for 2h, she suddenly developed severe chest pain which radiated to the left upper limb, left shoulder and left back. After 3h of ritodrine infusion, she developed chest tightness and chest pain. ECG showed acute anterior myocardial infarction (MI). [Extracted from the article]

After normal preoperative EKG, she was transferred to operating room and standard monitors, including noninvasive blood pressure, EKG, pulse oxygen saturation (SpO2), and bispectral index, were applied. Then norepinephrine infusion was initiated; however, ABP did not increase and ST-segment elevation followed by ventricular fibrillation was noted in the EKG (lack of efficacy). It was also concluded that, along with underlying variant angina, use of vasoconstrictors ephedrine, norepinephrine and epinephrine also contributed to the development of coronary spasm [ I time to reaction onset not stated i ]. [Extracted from the article]