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)

This is a case study of a 58-year-old patient with hypertrophic cardiomyopathy, mid-ventricular obstruction, and apical aneurysm who had an episode of syncope due to ventricular tachycardia. Cardiovascular magnetic resonance imaging revealed asymmetrical left ventricular hypertrophy with mid-ventricular obstruction and an apical aneurysm. His coronary angiography was normal, and his ventricular tachycardia was induced by hypertrophic cardiomyopathy without ischemia. Apical aneurysmectomy, left ventricular reconstruction, and cryoablation at the rim of the aneurysm were performed. Fifteen days after the operation, an automatic implantable cardioverter-defibrillator was implanted. The postoperative course was uneventful, and ventricular tachyarrhythmia did not recur during 18 months of follow-up.
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PMID:Hypertrophic cardiomyopathy with apical aneurysm: left ventricular reconstruction and cryoablation for ventricular tachycardia. 2154 32

After the initial evaluation including detailed history, physical examination, electrocardiogram, and orthostatic blood pressure measurements, risk stratification should follow, if the cause of syncope is still unclear in order to define the acuteness and extensiveness of the further diagnostic evaluation. The documentation of arrhythmia during syncope is the gold standard for diagnosis of arrhythmic syncope. The implantable loop recorder should be integrated early in the diagnostic work-up. In patients >40 years with otherwise unexplained syncope, carotid sinus massage is recommended. In suspected reflex-mediated syncope, the tilt test is able to confirm the diagnosis and gives information about the underlying pathomechanisms, while electrophysiological studies have still a proven indication in patients with previous myocardial infarction and preserved left ventricular function. The adenosine triphophate test has no clinical relevance in the diagnostics of syncope. Echocardiography plays an important role in the risk stratification by diagnosing structural cardiac disease. In patients experiencing syncope associated with exertion, exercise stress testing is indicated. Finally, a coronary angiogram should be performed, if ischemia triggered syncope is suspected. A routinely performed neurological evaluation is not recommended.
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PMID:[Significance of diagnostic methods in the work-up of syncope]. 2156 61

The pathophysiology of convulsive movements in patients with convulsive syncope remains unclear. Here, we report a patient with convulsive syncope whose convulsive movements seemed to be associated with transient hemodynamic ischemia in the basal ganglia. A 74-year-old man had 1-year history of orthostatic hypotension and transient clonic jerks in the limbs and trunk, predominantly in the right upper limb. His convulsive movements were evoked approximately 1 minute after sitting up or standing up from the supine position and lasted for several tens of seconds. He felt mild faint while the convulsive movements lasted, but he was oriented and could follow simple commands. He was diagnosed as pure autonomic failure. Video-electroencephalogram (EEG) recorded generalized slows without any epileptiform discharges when the symptoms appeared. Single-photon emission computed tomography (SPECT) was performed using split-dose method to evaluate the change in blood flow when the convulsive movements appeared. During symptoms, a significant decrease in blood flow was revealed in the anterior part of the left basal ganglia, bilateral frontal areas, and right cerebellar hemisphere. An alteration in the functional balance between the basal ganglia and the cerebral cortices may play a role in the generation of convulsive movements in patients with convulsive syncope.
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PMID:[Convulsive syncope associated with transient hemodynamic ischemia in the basal ganglia]. 2170 31

We report a case of anomalous origin of the left main coronary artery (LCA) from the noncoronary sinus of valsalva (LCANCS) in a young healthy patient who presented with syncope and cardiopulmonary arrest during exercise. The enhanced computed tomography showed acute angle take-off (AAT) of LCA, and the exercise stress thallium-201 myocardial scintigraphy demonstrated a large defect at the LCA perfusion region. We propose that the coexistence of AAT and resulting ischemia causes sudden cardiac death during exercise in the patients with LCANCS.
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PMID:Exercise-induced myocardial ischemia in a case of anomalous origin of the left main coronary artery from the noncoronary sinus of valsalva. 2177 65

Syncope is defined as a transient loss of consciousness due to cerebral hypoperfusion followed by spontaneous recovery. Common causes of syncope include vasovagal syncope, situational syncope, orthostatic hypotension, carotid sinus hypersensitivity, left- and right-sided obstructive cardiac lesions, and cardiac arrhythmias. History and physical examination often provide valuable clues about the underlying etiology of syncope. Admission decisions in the emergency department can be guided by various risk prediction scores. Evaluation of a patient with syncope involves a large battery of diagnostic tests that include a 12-lead electrocardiogram, Holter monitoring, echocardiogram, tilt table testing, ischemia evaluation, electrophysiologic studies, and other imaging tests. Despite the availability of these advanced diagnostic tests, a significant proportion of patients with syncope remain undiagnosed. Therapy should be tailored based on the underlying etiology of syncope.
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PMID:Syncope: Approaches to Diagnosis and Management. 2296 Aug 49

Rotational vertebral artery occlusion, or bow hunter's stroke, is reversible, positional symptomatic vertebrobasilar ischemia. The typical mechanism of action is obstruction of a dominant vertebral artery with contralateral head rotation in the setting of baseline ipsilateral vertebral artery stenosis or occlusion. Here we present a rare case of mechanical occlusion of bilateral patent vertebral arteries manifesting as near syncope with rightward head rotation. Diagnostic cerebral angiography showed dynamic right C5 vertebral occlusion and left C2 vertebral occlusion. The patient underwent right C4/5 transverse process decompression. Postoperative angiogram showed patent flow through the right vertebral artery in neutral position and with head turn with resultant resolution of symptoms.
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PMID:Bilateral mechanical rotational vertebral artery occlusion. 2346 74

Severe pallid breath-holding spells (BHSs) are based on parasympathetic hyperactivity, leading to cardiac asystole, pallor, brain ischemia, loss of consciousness, and reflex anoxic seizures. In recent years, an increasing number of patients with severe pallid BHSs have been successfully treated with pacemaker implantation. We present the case of a 13-month-old girl suffering from repeated severe pallid BHSs, causing asystole, loss of consciousness, and generalized anoxic seizures. She underwent treatment with oral glycopyrrolate, an anticholinergic drug, and an oral retard preparation of theophylline. The aim of the treatment was to decrease cardiac inhibition with glycopyrrolate and to bring about a positive chronotropic effect with theophylline. In our case, the combined therapy was effective in suppressing syncope and reflex anoxic seizures associated with BHSs This avoided the need for ventricular pacemaker implantation.
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PMID:Glycopyrrolate and theophylline for the treatment of severe pallid breath-holding spells. 2350 62

We report an extremely rare case of thebesian vein microfistulae to both ventricles. A 65-year-old woman, with no major cardiovascular risk factors, presented with multiple episodes of chest pain. The resting electrocardiogram showed T-wave inversion in leads V(1) -V(4). A Dipyridamole myocardial perfusion imaging revealed large and severe inferior defect with complete reversibility. Coronary angiography showed no coronary artery disease. On contrast injection, an exaggerated capillary blush from the distal portions of the right and left coronary artery systems was seen in both ventricles, mimicking the image of ventriculography. This appearance suggests prominent thebesian vessels, a congenital communication between the coronaries and the two ventricles. The clinical relevance of these myocardial sinusoids is still not well established. Although the majority of these fistulas are small in size and with no clinical significance, they can rarely present with chest pain, cardiac arrhythmia, syncope, myocardial infarction, and/or pulmonary hypertension. These fistulae when excessive can cause significant shunting of blood to the ventricles, leading to coronary steal phenomena and ischemia. This phenomenon is facilitated by the low resistance in these microfistulae as opposed to the higher resistance in the normal coronary circulation. Due to the diffuse nature of these microfistulae, neither surgery nor transcatheter therapy is feasible. This condition can only be managed medically; however, it should be noted that vasodilator agents, such as nitrates, can worsen the coronary steal phenomenon. Our patient was treated with ranolazine with significant improvement in her symptoms, which was not reported previously. Multiple coronary artery microfistulae could be an underestimated condition of angina in patient with normal coronaries.
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PMID:Persistent thebesian vessels involving the right and left ventricles leading to coronary steal phenomena and ischemia. 2366 1

A 67-year-old man who had a history of syncope was admitted because of effort angina. The sinus node (SN) was the single blood supply from the right coronary artery (RCA). After we implanted 2 everolimus-eluting stents for RCA, slow-flow occurred and the SN artery was occluded, and junctional escape rhythm was sustained. After the wiring to the occluded SN artery, junctional escape rhythm immediately recovered to sinus rhythm, and the patient achieved continuous sinus rhythm and stable hemodynamics. Given that acute SN ischemia is a possible cause of sinus dysfunction, careful choice of a percutaneous coronary intervention strategy should be taken into consideration if the SN artery is the single blood supply from the RCA and if syncopal history is present.
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PMID:Sinus dysfunction after stent implantation in the right coronary artery immediately recovered after reflow in the sinus node artery. 2403 71

Long QT syndrome (LQTS) is a congenital abnormality of cardiac repolarization that manifests as a prolonged QT interval on 12-lead electrocardiograms (ECGs). The syndrome may lead to syncope and sudden death from ventricular tachyarrhythmias known as torsades de pointes. An increased persistent Na(+) current is known to cause a Ca(2+) overload in case of ischemia for example. Such increased Na(+) persistent current is also usually associated to the LQT3 syndrome. The purpose of this study was to investigate the pathological consequences of a novel mutation in a family affected by LQTS. The impact of biophysical defects on cellular homeostasis are also investigated. Genomic DNA was extracted from blood samples, and a combination of PCR and DNA sequencing of several LQTS-linked genes was used to identify mutations. The mutation was reproduced in vitro and was characterized using the patch clamp technique and in silico quantitative analysis. A novel mutation (Q1476R) was identified on the SCN5A gene encoding the cardiac Na(+) channel. Cells expressing the Q1476R mutation exhibited biophysical alterations, including a shift of SS inactivation and a significant increase in the persistent Na(+) current. The in silico analysis confirmed the arrhythmogenic character of the Q1476R mutation. It further revealed that the increase in persistent Na(+) current causes a frequency-dependent Na(+) overload in cardiomyocytes co-expressing WT and mutant Nav1.5 channels that, in turn, exerts a moderating effect on the lengthening of the action potential (AP) duration caused by the mutation. The Q1476R mutation in SCN5A results in a three-fold increase in the window current and a persistent inward Na(+) current. These biophysical defects may expose the carrier of the mutation to arrhythmias that occur preferentially in the patient at rest or during tachycardia. However, the Na(+) overload counterbalances the gain-of-function of the mutation and is beneficial in that it prevents severe arrhythmias at intermediate heart rates.
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PMID:Sodium overload due to a persistent current that attenuates the arrhythmogenic potential of a novel LQT3 mutation. 2409 84


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