Prinzmetal's Variant Angina Associated With Subarachnoid Hemorrhage: A Case Report

Toyama, Yoshifumi; Tanaka, Hiromitsu; Nuruki, Kohji; Shirao, Tetsuya

doi:10.1177/000331977903000311

Cited by 17 publications

(7 citation statements)

References 46 publications

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“…33 Although reversible myocardial contractile dysfunction ("stunning") can also result from ischemia associated with coronary artery atherosclerosis or vasospasm, 2 this process would be expected to correspond closely to one or more arterial territories. Coronary artery vasospasm has been postulated as a possible mechanism of cardiac injury in SAH, 43,47 but has never been documented. Nontransmural subendocardial infarction related to microvascular compromise and increased myocardial demand may also explain the clinical findings in our patients, and in one autopsy study was identified as the cause of apical septal hypokinesis in a patient with SAH.…”

Section: Mechanism Of Neurogenic Cardiac Injurymentioning

confidence: 99%

Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage

Mayer¹,

Limandri²,

Sherman³

et al. 1995

Journal of Neurosurgery

165

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A reversible and presumably neurogenic form of myocardial dysfunction may occur following subarachnoid hemorrhage (SAH), but the relationship of this finding to electrocardiographic abnormalities remains unclear. To clarify this issue, serial electrocardiograms (ECGs, mean 6.2 per patient) and echocardiograms (mean 3.4 days after SAH) were obtained in 57 SAH patients without preexisting cardiac disease. The goal was to determine which specific electrocardiographic changes, if any, reflect abnormal left ventricular wall motion in acute SAH. Wall motion abnormalities were identified in five (8%) of 57 patients. Four of these affected patients experienced hypotension (systolic blood pressure < 100 mm Hg) and three exhibited pulmonary edema within 6 hours of SAH, compared to none of the 52 patients with normal wall motion (p < 0.0001). Patients with abnormal wall motion were more likely than patients with normal echocardiograms to have symmetrical T wave inversion (five of five vs. seven of 52, p < 0.001) and severe (> or = 500 msec) QTc segment prolongation (five of five vs. three of 52, p < 0.001) on serial ECGs. These associations maintained their significance with analysis limited to single ECGs performed on or near the day of echocardiography. Abnormal wall motion was also associated with borderline (2% to 5%) creatine kinase MB elevation (five of five vs. three of 52, p < 0.001) and poor neurological grade (p < 0.0001). Although no combination of findings on a single ECG resulted in 100% sensitivity for abnormal wall motion, the presence of either inverted T waves or severe QTc segment prolongation on serial ECGs was associated with 100% sensitivity and 81% specificity. These results demonstrate an association between reduced left ventricular systolic function, mild creatine kinase MB elevation, and electrocardiographic repolarization abnormalities in acute SAH. Symmetrical T wave inversion and severe QTc segment prolongation best identified patients at risk for myocardial dysfunction and may serve as useful criteria for echocardiographic screening following SAH.

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Section: Mechanism Of Neurogenic Cardiac Injurymentioning

confidence: 99%

Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage

Mayer¹,

Limandri²,

Sherman³

et al. 1995

Journal of Neurosurgery

165

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“…Other authors have described a case of Prinzmetal's angina associated with subarachnoid hemorrhage. 7 Our case, however, illustrates that, in rare instances, myocardial injury can follow damage to the rostral ventrolateral medulla. We felt surgery was not contraindicated because of the normal findings on coronary angiogram but a risk of increased harm existed.…”

mentioning

confidence: 62%

Myocardial injury after hemorrhage into the lateral medulla oblongata

Rogers¹,

Phan²,

Wijdicks³

2001

Neurology

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Myocardial injury patterns in acute disorders of the central nervous system vary from transient cardiac stunning to primarily subendocardial myonecrosis. 1 Myocardial injury has been attributed to sympathetic overdrive. Coronary vasospasm may be implicated in some patients without coronary artery disease. We report a patient without significant coronary artery disease who developed myocardial injury after a medullary hemorrhage.Case report. A 48-year-old woman presented with the sudden onset of nausea, vertigo, and diplopia. She described environmental "tilting," which worsened when standing. Her left arm became numb and clumsy 1 hour after these symptoms began.On admission, her pulse rate was 90 beats/min and her blood pressure was 140/70 mm Hg. Cardiovascular examination was normal. Pupils were equal in size, symmetric, and reacted briskly. Fundoscopy findings were normal. Extraocular movements showed saccadic pursuits, and counterclockwise rotatory nystagmus was present on primary gaze. Mild hypoesthesia was found over the left side of the face, with loss of the corneal reflex. A left central facial nerve paresis was present. Other cranial nerves were intact, including pharyngeal sensation and movement. Muscle tone, and power and stretch reflexes were normal. Left upper extremity sensation to superficial pain was decreased. Truncal ataxia was evident in the seated position, and the patient's left arm and leg were ataxic.The following morning, the patient had epigastric pain. Her neurologic examination showed new palatal and pharyngeal weakness. Speech had become hypophonic, and the gag reflex was diminished. An urgent MRI/MR angiography of the head with axial fluid attenuated inversion recovery, and diffusion-weighted and gradient echo images disclosed a 1.2-cm hemorrhage in the left medulla. Appearance was consistent with an acute hemorrhage into a preexisting cavernous hemangioma (figure 1).Several hours later, the patient became tachycardic (120 beats/ min) and developed hypertension (210/90 mm Hg), a new headache, and more severe epigastric pain. Electrocardiogram (ECG) revealed a bigeminal rhythm with peaked T waves and mild STsegment depression in inferolateral leads (figure 2). Cardiac enzymes were elevated: creatine kinase (CK)-MB 19.7 (normal Յ 4.3 ng/mL) and CK-MB fraction 10.2 (normal Ͻ1.3%). Initially, troponin I was normal at 0.4 (normal Ͻ0.5 ng/mL), but rose to 3.3 the following day. Transthoracic echocardiogram showed regional wall motion abnormalities in the inferoseptal wall and the posterolateral ventricle. This had changed from the transesophageal echocardiogram performed on admission, which had revealed normal left ventricular function and no regional wall motion abnormalities. Figure 1. Axial T2-weighted and axial gradient echo MR images of the brain showing a left medullary hemorrhage (arrow).Figure 2. (A) Electrocardiogram (ECG) on admission with minimal ST segment depression and regular sinus rhythm pattern in V 1 . (B) ECG with epigastric pain, showing bigeminal rhythm, peaked T waves ...

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“…One of the possible mechanisms of cardiac dysfunction is ischemia resulting from coronary thrombosis or epicardial coronary artery spasm [36,37]. Another possible mechanism is microvascular vasospasm because microvascular vasospasm or dysfunction could not be evaluated angiographically.…”

Section: Discussionmentioning

confidence: 99%

Are Electrocardiographic Changes in Patients with Acute Subarachnoid Hemorrhage Associated with Takotsubo Cardiomyopathy?

et al. 2009

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Background: Subarachnoid hemorrhage (SAH) has been associated with electrocardiographic (ECG) changes, arrhythmias, and release of cardiac enzymes. Recently, Takotsubo cardiomyopathies, presenting typical ECG changes and left ventricular (LV) regional wall-motion abnormalities (RWMAs), have been reported and considered to be a result of high norepinephrine (NE) levels. We hypothesized that ST-T-wave changes in patients with SAH may be manifestations of Takotsubo cardiomyopathy and associated with RWMAs. Methods: We instituted consecutive echocardiographic screening of all patients with acute aneurysmal SAH. A standard 12-lead ECG and blood samples for creatine kinase (CK) MB isoenzyme and troponin-T (Tn-T) were obtained. To evaluate sympathetic nervous activity, we obtained blood samples and urine samples for NE. Results: Of 42 patients with acute aneurysmal SAH, 26 had abnormal ECG including rhythm abnormalities. Ten of 12 patients with ST-T-wave changes had severe neurologic deficits, but 1 patient had RWMAs on echocardiography. Another patient with LV dysfunction showed a normal ST-T wave. In patients with ST-T-wave changes, elevated Tn-T (8.3 vs. 3.3%), CK-MB (8.3 vs. 10.0%), plasma and urine NE (16.7 and 33.3% vs. 16.7 and 50.0%), and mortality (8.3 vs. 13.3%) were not significantly higher. All 5 deaths resulted from noncardiac causes. High plasma and urine NE levels were not related to neurologic severity or mortality. Conclusions: Although ECG abnormalities are frequently seen in SAH patients, the incidence of RWMAs is very low. Electrocardiographic manifestations in patients with SAH and Takotsubo cardiomyopathy are similar, but ECG abnormalities in patients with SAH are mostly not related to LV dysfunction.

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Prinzmetal's Variant Angina Associated With Subarachnoid Hemorrhage: A Case Report

Cited by 17 publications

References 46 publications

Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage

Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage

Myocardial injury after hemorrhage into the lateral medulla oblongata

Are Electrocardiographic Changes in Patients with Acute Subarachnoid Hemorrhage Associated with Takotsubo Cardiomyopathy?

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