Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac and noncardiac side effects were studied in 293 consecutive patients referred for nonexercise stress thallium imaging with intravenous dipyridamole. Six minutes after the initiation of infusion, there was a mean 9-beat/min increase in heart rate and a mean 12-mm Hg decrease in systolic blood pressure. The largest increase in heart rate exceeded 20 beats/min in only 13% of patients and the largest decrease in systolic blood pressure exceeded 20 mm Hg in 31%. Noncardiac side effects were headache (11%), lightheadedness or dizziness (5%) and nausea (4%). Only 9 patients required intravenous aminophylline for relief of noncardiac side effects: severe headache in 7 and nausea in 2. Cardiac side effects included chest pain in 76 patients (26%), of whom 70% were given aminophylline for relief of symptoms. Sixty patients (20%) had ischemic ST-segment depression and 56 (19%) had arrhythmias (ventricular in 50 and atrial in 6). There were no deaths, myocardial infarctions or sustained arrhythmias due to dipyridamole administration. Among 62 patients also undergoing cardiac catheterization, side effects except for arrhythmias were unrelated to the number of vessels with coronary artery disease. Intravenous dipyridamole is safe for nonexercise stress testing and has few serious side effects. However, the possibility of ischemia requires careful selection of patients and monitoring of vital signs and the electrocardiogram during the test.
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PMID:Safety of intravenous dipyridamole for stress testing with thallium imaging. 381 27

A 78-year-old right-handed man with idiopathic orthostatic hypotension and a history of Hashimoto's thyroiditis presented over 2 years with recurrent, stereotyped attacks of bilateral limb shaking and metamorphopsia, which were precipitated by standing more than 3 or 4 minutes, or walking a few meters. These symptoms would resolve upon squatting or lying down and did not occur spontaneously at rest. He did not lose consciousness during the attacks. Speech, power, and sensation were preserved during these attacks. He had no history of seizures or habit of smoking. On examination, his supine blood pressure was 110/60 mmHg, and 62/27 mmHg on standing, with the pulse rate being 61/min and 66/min, respectively. Although he showed orthostatic hypotension, he did not complain of fainting or lightheadedness on standing alone. Magnetic resonance imaging of the brain revealed mild periventricular white matter changes and multiple small ischemic lesions bilaterally in the cerebral deep white matter. An electroencephalogram (EEG) showed mild, generalized slowing of nonspecific feature. EEG monitoring during a limb shaking episode showed no epileptiform abnormalities. Cerebral angiogram revealed a moderate degree of stenosis of the left internal carotid and a mild degree of stenosis of the right internal carotid, the right vertebral arteries and the left vertebral arteries. A single-photon emission computed tomography (SPECT) showed a moderate compromise of perfusion of the left internal carotid territory. After managing both hypotension and orthostatic hypotension with antihypotensive medication and levothyroxine sodium, his symptoms dramatically disappeared. Thus, we diagnosed that transient hemodynamic insufficiency due to combination of vascular stenosis and hypotension was the cause of these symptoms. Limb shaking is a well-described presentation of carotid artery occlusive disease and is usually unilateral. Bilateral limb shaking is rare and only 2 cases have been reported. Metamorphopsia is also a rare symptom of vertebrobasilar ischemia. We suggest that bilateral limb shaking correlates with hypoperfusion in the anterior border zones and metamorphopsia with that in the posterior border zones of both hemispheres. Hemodynamic TIA should be considered as a cause of movement disorders affecting four limbs.
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PMID:[Orthostatic hypotension with repeated bilateral limb shaking and metamorphopsia. A case of hemodynamic transient ischemic attacks]. 1108 97

We present a 46-year-old patient who suffered from cardiac arrest and subsequently underwent placement of an implantable cardioverter defibrillator (ICD). The patient underwent a cardiac catheterization which revealed no significant coronary artery disease. About 1 year later he experienced appropriated and frequent ICD discharges due to monomorphic ventricular tachycardia (VT) with left bundle branch block morphology. His prodromal symptoms were mild dizziness and lightheadedness with no chest pain. Amiodarone, mexiletine, sotalol and dofetilide as well as ablation of two inducible ventricular tachycardias in the electrophysiology studies were unsuccessful in controlling the arrhythmias and ICD discharges. During the last episode, he experienced a mild burning sensation in his chest and was given nitroglycerin 0.4 mg sublingually, which relived his symptoms and aborted the VT. This led to a second cardiac catheterization to investigate whether the VT was being induced by myocardial ischemia. This second coronary angiogram spontaneously revealed significant coronary vasospasm and simultaneously, the patient's cardiac rhythm showed short runs of VT with left bundle branch block morphology. Intracoronary nitroglycerine relieved the coronary vasospasm and terminated the arrhythmia. The patient was treated with isosorbide mononitrate and diltiazem. He remained symptom free with no ICD discharges and no VT in ICD interrogations for more than 2 years. Coronary vasospasm may be silent and with no chest pain which creates a difficult clinical situation particularly if it is associated with ventricular tachycardia and sudden cardiac death. The mechanisms of VT in the setting of coronary vasospasm are not known and increased automaticity, focal discharges, functional unidirectional block with reentry, or a combination of these mechanisms may contribute to inducing the VT during the transient ischemia or rarely in the reperfusion phase. It is important to perform provocative tests to diagnose silent coronary vasospasm in unexplained sudden cardiac arrests.
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PMID:Multiple episodes of ventricular tachycardia induced by silent coronary vasospasm. 1829 82

Acute coronary syndrome and myocardial infarction have been described to present with atypical symptoms in certain subsets of patients. However, these subsets commonly do not include middle-aged males with a paucity of underlying medical conditions. We present a very unique case of acute coronary syndrome in a 53-year-old male, with no previously identified medical conditions other than chronic back pain. The patient was encountered by rural emergency medical service providers presenting with syncope followed by intermittent episodes of lightheadedness. Further, electrocardiographic changes consistent with acute ischemia could only be demonstrated with the patient in a standing position, prior to the development of an occurrence of ventricular tachycardia, which degenerated into ventricular fibrillation. To our knowledge, this is a very rare case of electrocardiographic changes consistent with occult, acute cardiac ischemia with a proven coronary artery lesion seen initially only with the patient in a standing position.
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PMID:Acute coronary ischemia identified by EMS providers in a standing middle-aged male with atypical symptoms. 2460 73

The cervical vertebral arteries were visualized by real-time B-mode ultrasonography with duplex Doppler in 595 consecutive patients. Comparison with angiography in 40 patients showed a sensitivity of 84% and a specificity of 97% in identifying vertebral artery lesions. The incidence of vertebral artery lesions in patients with symptoms of ischemia referable to the vertebrobasilar distribution was 28% (24/84), significantly higher (p = 0.05) than the incidence of 13% (7/54) in patients with carotid artery insufficiency. Patients with completed strokes in the vertebrobasilar territory had an even higher incidence of vertebral lesions (44%,14/ 32) than patients with transient symptoms of vertebrobasilar insufficiency (19%, 10/52) (p < 0.001). The incidence of vertebral lesions in patients with nonlocalizing symptoms of syncope (8%, 5/67), presyncope (10%, 3/31), isolated vertigo (5%,4/77), unsteadiness (4%,2/55), lightheadedness (0/27), and transient global amnesia (0/18) were all significantly lower than the incidence in patients with focal vertebrobasilar symptoms (p < 0.01). Imaging of the cervical vertebral arteries by real-time B-mode ultrasonography may be helpful in determining the etiology of symptoms in patients with a diagnosis of vertebrobasilar insufficiency.
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PMID:Noninvasive imaging of the cervical vertebral artery in the diagnosis of vertebrobasilar insufficiency. 2648 22

Medications for opioid use disorder (MOUD) and opioid agonist therapy (OAT) are the mainstays of treatment in opioid use disorder. Significant caution is encouraged upon initiation to reduce the precipitation of opioid withdrawal. Cardiac events in the setting of opioid withdrawal are rare and incompletely understood. A 46-year-old woman with a history of opioid-use disorder, hypertension, hyperlipidemia, diabetes, tobacco-use disorder, and rheumatoid arthritis presented with nausea, vomiting, and lightheadedness after taking naltrexone following buprenorphine. She was found to be hypertensive and tachycardic in the emergency department, with a troponin of 0.38 ng/mL (reference: 0.00-0.30 ng/mL) and an electrocardiogram (ECG) without ST or T-wave changes. She was admitted for a non-ST-elevation myocardial infarction (NSTEMI) and hypertensive emergency in the setting of opioid withdrawal. Her blood pressure was controlled, and she received full-dose aspirin and high intensity atorvastatin. Afterwards she was started on a modified OAT regimen of buprenorphine 8 mg daily. Her cardiac enzymes down-trended and her condition became stable after which she was discharged home. Cardiac events are an uncommon yet lethal occurrence in opioid withdrawal. The likely etiology of NSTEMI in our patient was demand ischemia induced by opioid withdrawal, augmented by her various other cardiac risk factors. Practitioners should be aware of these possible adverse events, especially in those with preexisting cardiac disease. Meticulous efforts should be made to instruct patients as to the proper dosing schedule when initiating opioid therapy, and when initiating MOUD/OAT in order to prevent poor outcomes.
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PMID:Naltrexone-Associated Non-ST-Elevated Myocardial Infarction. 3326 29