Peer Reviewed

Photo Essay

A Series of Cases Involving Cardiometabolic Disease and Related Conditions

Reversible Posterior Leukoencephalopathy Syndrome With Hypertensive Emergency

Ian Quinn, BS, OMS-III, and Taral R. Sharma, MD, MBA
Edward Via College of Osteopathic Medicine, Spartanburg, South Carolina

Quinn I, Sharma TR. Reversible posterior leukoencephalopathy syndrome with hypertensive emergency. Consultant. 2017;57(5, Suppl.):S11-S12.


A 71-year-old woman presented to the emergency department (ED) with nausea, diarrhea, altered mental status, and loss of vision in both eyes. She had a history of type 2 diabetes mellitus, chronic obstructive pulmonary disease, coronary artery disease, deep vein thrombosis with pulmonary embolism, and uncontrolled hypertension

The patient had started to experience nausea with some dry heaving but without vomiting, along with diarrhea 5 days ago. The next day, she visited her primary care provider, who prescribed an antiemetic; after several more days, the symptoms had not improved, and she decided to come to the ED, where she rapidly developed decreased sight and loss of mentation. In the ED, her systolic blood pressure was above 190 mm Hg. Upon arrival, she was able to answer questions, but soon after she became unresponsive. Her husband, who accompanied her to the ED, stated that nothing like this had occurred previously, and he did not remember any other problems with vision or mentation in his wife’s past.

Physical examination. Upon admission, the patient’s temperature was 36.5°C, her respiratory rate was 18 breaths/min, her pulse was 108 beats/min, and her blood pressure was 160/102 mm Hg. She would respond to loud verbal cues but was unable to be understood. She could open her eyes when asked but was incapable of keeping them open, and she was not oriented to person, place, or time.

Her pupils were equally round and reactive to light. She was without any obvious neurologic deficits, including facial droop, cranial nerve palsies or distal paralysis, paresis, and paresthesia, although these were difficult to assess. She had tachycardia with a regular rhythm, and lungs sounds were clear to auscultation.

RPLS figure 1

Diagnostic tests. The results of laboratory tests, including a complete blood cell count, a comprehensive metabolic panel, prothrombin time, and international normalized ratio, were almost completely within normal limits, except for a decreased hemoglobin of 9.7 g/dL. An electrocardiogram showed no acute changes, and chest radiography findings were unremarkable. A computed tomography (CT) scan of the head without contrast was ordered in an attempt to rule out acute intracranial pathologies, and the results showed no significant findings such as intracerebral hemorrhage or ischemia (Figure 1). The CT scan was followed quickly with magnetic resonance imaging (MRI) of the head with and without contrast, the results of which showed diffuse signals in the occipital temporal regions bilaterally and patchy areas in the frontoparietal regions consistent with reversible posterior leukoencephalopathy syndrome (RPLS) (Figure 2).

RPLS figure 2

Based on her presentation and diagnostic test findings, she was admitted to the intensive care unit, where she was maintained on a nicardipine drip to achieve a systolic blood pressure below 140 mm Hg and levetiracetam intravenously twice daily to prevent seizures. In spite of these treatments, the patient did have a seizure during her first night in the hospital, which resolved with a single dose of lorazepam. The next day, the patient started to show improvement in mental status and vision, but she did express signs of Anton syndrome that morning.

Outcome of the case. Several days later, the patient was able to read a newspaper and was alert and oriented to person, place, and time. She was discharged home in stable condition, with outpatient physical therapy twice weekly and scheduled follow-up with her primary care provider in 1 week.

Discussion. RPLS (also called posterior reversible encephalopathy syndrome, or PRES) was first described by Hinchey and colleagues1 in 1996 as a clinical and radiologic syndrome characterized by a reversible, predominantly posterior leukoencephalopathy associated with a cluster of signs and symptoms, including headache, vomiting, confusion, seizures, cortical blindness, other visual abnormalities, and motor signs.2,3 Fugate and Rabinstein4 summarized the main clinical symptoms of RPLS in adults as follows: encephalopathy (50%-80% of cases), seizures (60%-75%), headache (50%), visual disturbances (33%), focal neurologic deficit (10%-15%), and status epilepticus (5%-15%). Hypertension is considered the primary risk factor for the development of RPLS, along with eclampsia of pregnancy, kidney disease, and other etiologies unrelated to hypertension such as immunosuppressive medication use, sepsis, and autoimmune diseases.2,5,6

The fact that symptoms are not specific to RPLS highlights the importance of a focused clinical approach, along with advanced CT and MRI.3,7-9 The symmetric location of the edema on brain MRI, along with the increased diffusion signal in the apparent diffusion coefficient maps, helps differentiate vasogenic edema from cytotoxic edema (which has restricted diffusion). Multiple areas of edema in the brain can be seen on MRI in many situations such as metastasis, stroke, and encephalitis.

RPLS is a rare but severe clinical condition with potentially reversible causes. When a patient presents with clinical findings suggestive of RPLS, clinicians should promptly proceed to neuroimaging. If the characteristic imaging features are evident, the diagnosis of RPLS can be confirmed, and treatment should be started immediately.

Although RPLS is not malignant, its prognosis varies due to several factors. In the largest series of 70 patients with RPLS published to date, 16% of patients died, 37% had marked functional impairment, and only 56% had a satisfactory recovery.10 The clinical factors that are independently associated with poor prognosis are the time needed to control the causative factor and the degree of glycemia on admission10; the radiologic factors related to poor prognosis (although controversial) are the irreversibility of the lesions and the presence of hemorrhage.11,12

While RPLS may be an easily identified syndrome by a radiologist, its constellation of symptoms is not as readily recognized by primary care providers. While the exact mechanism of the disease has not been definitively identified, it is believed to be related to significant increases in blood pressure, especially acutely. Rapid diagnosis, controlled lowering of blood pressure, and preventing or treating seizures are incredibly important to increase the likelihood of a favorable outcome.

In our patient’s case, severe hypertension was the precipitating factor for RPLS, and it was paramount to have a prompt but controlled reduction in her blood pressure. Since a time greater than 30 minutes to control the causative factor of RPLS onset triples the chances for a poor prognosis,10 it is crucial to intervene acutely and aggressively (although the optimal levels or ways of blood pressure reduction have not been clearly documented). 


  1. Hinchey J, Chaves C, Appignani B, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med. 1996;334(8):494-500.
  2. Lee VH, Wijdicks EFM, Manno EM, Rabinstein AA. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Arch Neurol. 2008;65(2):​205-210.
  3. Bartynski WS. Posterior reversible encephalopathy syndrome, part 1: fundamental imaging and clinical features. AJNR Am J Neuroradiol. 2008;29(6):​1036-1042.
  4. Fugate JE, Rabinstein AA. Posterior reversible encephalopathy syndrome: clinical and radiological manifestations, pathophysiology, and outstanding questions. Lancet Neurol. 2015;14(9):914-925.
  5. Bartynski WS, Boardman JF, Zeigler ZR, Shadduck RK, Lister J. Posterior reversible encephalopathy syndrome in infection, sepsis, and shock. AJNR Am J Neuroradiol. 2006;27(10):2179-2190.
  6. Amagada JO, Kondagunta H, Afshan N, Watermeyer S, Jones R. Posterior reversible encephalopathy syndrome secondary to eclampsia. J Obstet Gynaecol. 2008;28(6):646-647.
  7. Hugonnet E, Da Ines D, Boby H, et al. Posterior reversible encephalopathy syndrome (PRES): features on CT and MR imaging. Diagn Interv Imaging. 2013;94(1):45-52.
  8. Benoist G, Dossier C, Elmaleh M, Dauger S. Posterior reversible encephalopathy syndrome revealing renal artery stenosis in a child. BMJ Case Rep. 2013;2013. doi:10.1136/bcr-2013-010110
  9. Fugate JE, Claassen DO, Cloft HJ, Kallmes DF, Kozak OS, Rabinstein AA. Posterior reversible encephalopathy syndrome: associated clinical and radiologic findings. Mayo Clin Proc. 2010;85(5):427-432.
  10. Legriel S, Schraub O, Azoulay E, et al; Critically III Posterior Reversible Encephalopathy Syndrome Study Group (CYPRESS). Determinants of recovery from severe posterior reversible encephalopathy syndrome. PLoS One. 2012;7(9):e44534.
  11. Moon S-N, Jeon SJ, Choi SS, et al. Can clinical and MRI findings predict the prognosis of variant and classical type of posterior reversible encephalopathy syndrome (PRES)? Acta Radiol. 2013;54(10):1182-1190.
  12. Alhilali LM, Reynolds AR, Fakhran S. A multi-disciplinary model of risk factors for fatal outcome in posterior reversible encephalopathy syndrome. J Neurol Sci. 2014;347(1-2):59-65.


NEXT: Bullosis Diabeticorum

Bullosis Diabeticorum

Thinzar Lin, MD; Poras Patel, MD; Aung Naing Lin, MD; Santosh Sharma, MD; Iqbal Singh, MD; and Kyawzaw Lin, MD
The Brooklyn Hospital Center, Affiliate of Mount Sinai Hospital/Icahn School of Medicine at Mount Sinai, Brooklyn, New York

Aye Aye Lwin, FRCP
University of Medicine, Mandalay, Myanmar

Lin T, Patel P, Lin AN, Sharma S, Singh I, Lin K, Lwin AA. Bullosis diabeticorum. Consultant. 2017;57(5, Suppl.):S13-S14.


A 78-year-old woman presented with a sudden onset of numerous blisters of various sizes on both feet that had developed earlier that morning. She had uncontrolled type 2 diabetes mellitus complicated by neuropathy, along with multiple comorbidities including hyperlipidemia, hypertension, and osteoarthritis.

History. The patient reported no history of trauma, recent insect bites, traveling or camping, changes in medications or cosmetics, or use of alcohol or illicit drugs. She denied fever, chills, vomiting, diarrhea, abdominal pain, change in urine color, or symptoms suggestive of infection and inflammation.

Physical examination. Multiple painful cystic bullae ranging from 4 to 8 cm in diameter were present on the dorsal and plantar surfaces of the patient’s feet bilaterally (Figures). The skin on the floors of the bullae appeared normal. No signs of infection were present.

Bullosis Diabeticorum figures

She was admitted to the hospital with a suspected diagnosis of bullous pemphigoid and underwent extensive workup, including numerous blood tests. Oral prednisone was begun empirically, along with topical antibiotics. However, her condition had not improved after 5 days of treatment, and her blood glucose levels were erratic as a result of the corticosteroids.

Diagnostic tests. She then underwent drainage of the bullae, and the lesions and surrounding skin were biopsied. Wound culture grew normal skin flora, which was considered to be contamination. The biopsy results of one of the lesions showed ulcerations featuring subcutaneous hyalinized microangiopathy, suggesting an ischemic etiology. The results of the 7 other biopsies from other lesions confirmed this finding. Ultimately, the diagnosis of bullosis diabeticorum (BD) was made based on clinical and histologic features.

Discussion. BD, or bullous disease of diabetes mellitus, is a rare condition characterized by the abrupt formation of noninflammatory, tense, and painless subepidermal bullae. It is a rare cutaneous complication of diabetes mellitus and commonly develops on the upper and lower extremities of persons with diabetes or prediabetes.1

BD was first described by Kramer in 19302 and was first named bullosis diabeticorum by Cantwell and Martz in 1967.3 It is a rare cutaneous manifestation of diabetes mellitus, occurring in only approximately 0.5% of the US population with diabetes mellitus.4,5 Male patients are twice as likely to develop BD than are female patients.1

Blisters filled with sterile serosanguineous fluid and with noninflammatory bases on the dorsum of acral skin, measuring up to several centimeters in diameter, are typical features of BD.6 The pathophysiology is poorly understood; however, some believe that poor vascular circulation and elevated venous pressure lead to splitting of the dermal-epidermal junction and formation of blisters.7

The diagnosis of BD typically is made based on its characteristic appearance, location, and clinical course in the context of diabetes. The bullae of BD often are mistaken for symptoms of an autoimmune disease such as pemphigoid, and patients with BD often unnecessarily undergo immunosuppressive therapy. Other possible etiologies that can mimic the presentation of BD include drug eruption, porphyria cutanea tarda, acquired epidermolysis bullosa, and bullous impetigo.

The course of disease is benign and self-limiting, with lesions generally resolving spontaneously in 2 to 6 weeks, but the recurrence rate is high.8 In one retrospective study of 25 patients with BD treated over a 3-year period, the reported median healing time was 2.5 months (range 0.5-23 months).8 If lesions persist more than a few weeks, biopsy of bullae should be considered to rule out bullous pemphigoid and other etiologies.

Management consists mainly of aspiration of bullae, application of topical antibiotics, and regular dressing changes to prevent secondary infection, ulceration, and necrosis.9 Because BD can be a painless condition in a patient with diabetic peripheral neuropathy, it is crucial for all persons with diabetes to have periodic diabetic foot care and to be educated about the importance of proper foot care and strict glycemic control. Tight glycemic control and prevention of secondary bacterial infections have been shown to contribute to more rapid improvement of BD and a reduction in its recurrence rate.

Outcome of the case. After other possible etiologies had been ruled out and histopathologic test results had confirmed the diagnosis of BD, the patient was managed conservatively with strict glycemic control and supportive care, with daily sterile dressing of the deroofed blisters. At an outpatient follow-up visit 1 week after discharge, significant clinical improvement had occurred in her skin lesions, without any evidence of scar formation.


  1. Riad H, Al Ansari H, Mansour K, et al. Pruritic vesicular eruption on the lower legs in a diabetic female. Case Rep Dermatol Med. 2013;2013:​641416.
  2. Kramer DW. Early or warning signs of impending gangrene in diabetes. Med J Rec. 1930;132:338-342.
  3. Cantwell AR Jr, Martz W. Idiopathic bullae in diabetics: bullosis diabeticorum. Arch Dermatol. 1967;96(1):42-44.
  4. Gupta V, Gulati N, Bahl J, Bajwa J, Dhawan N. Bullosis diabeticorum: rare presentation in a common disease. Case Rep Endocrinol. 2014;2014:​862912.
  5. Lopez PR, Leicht S, Sigmon JR, Stigall L. Bullosis diabeticorum associated with a prediabetic state. South Med J. 2009;102(6):643-644.
  6. Mims L, Savage A, Chessman A. Blisters on an elderly woman’s toes. J Fam Pract. 2014;63(5):273-274.
  7. Lipsky BA, Baker PD, Ahroni JH. Diabetic bullae: 12 cases of a purportedly rare cutaneous disorder. Int J Dermatol. 2000;39(3):196-200.
  8. Larsen K, Jensen T, Karlsmark T, Holstein PE. Incidence of bullosis diabeticorum—a controversial cause of chronic foot ulceration. Int Wound J. 2008;​5(4):591-596.
  9. Mascaró JM Jr. Other vesiculobullous diseases. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 1. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012:515-522.


NEXT: Takotsubo Cardiomyopathy

Takotsubo Cardiomyopathy

Igor Wroblewski, MD; Mahmoud Khreis, MD; Diana Carolina Miranda Ruiz, MD; and Shyam Chalise, MD
Presence Saint Joseph Hospital, Chicago, Illinois

Wroblewski I, Khreis M, Ruiz DCM, Chalise S. Takotsubo cardiomyopathy. Consultant. 2017;57(5, Suppl.):S14-S16.


A 59-year-old man was referred to our hospital for evaluation after a fall and loss of consciousness. His past medical history included hypertension and atrial fibrillation. He was a heavy alcohol drinker (3 glasses of liquor daily); his last drink had been 2 days prior to presentation. After his fall, he had been found sitting on the ground, confused, without recollection of what had happened.

Physical examination. The patient’s vital signs were as follows: temperature, 36.4°C; blood pressure, 160/115 mm Hg; pulse rate, 123 beats/min; respiration rate, 18 breaths/min; and oxygen saturation, 95% on room air. Physical examination findings were significant for signs of malnutrition, confusion, restlessness, and tremulousness, as well as a laceration on the mucosa of the lower lip.

Diagnostic tests. Laboratory test results revealed electrolyte abnormalities, including a potassium level of 3.0 mEq/L (reference range, 3.5-5.1 mEq/L), a chloride level of 95 mEq/L (reference range, 98-107 mEq/L), a magnesium level of 1.4 mg/dL (reference range, 1.6-2.6 mg/dL), and a phosphorus level of less than 1.0 mg/dL (reference range, 2.5-5.0 mg/dL).

Computed tomography (CT) scans of the head revealed no acute intracranial abnormalities (ie, no acute territorial infarction, focal mass lesion, or midline shift). Electroencephalography (EEG) findings were unremarkable.

An electrocardiogram (ECG) recorded sinus tachycardia and T-wave inversion in the anterior leads. The troponin I level was elevated at 0.68 ng/mL (reference value, < 0.05 ng/mL), with subsequent values trending upward and achieving a peak of 0.82 ng/mL. A follow-up ECG showed deep T-wave inversion in precordial leads V3 through V5 (Figure 1).

Takotsubo Cardiomyopathy figure 1
The patient’s ECG showing T-wave inversion in precordial leads V3 through V5.


Results of transthoracic echocardiography showed severe anterior and apical wall hypokinesis. He subsequently underwent coronary angiography during left-heart catheterization, which disclosed normal epicardial coronary arteries (Figure 2). Results of left ventriculography revealed depressed left ventricular  (LV) systolic function with apical akinesis and a LV ejection fraction of 35% (Figure 3), findings suggestive of takotsubo cardiomyopathy (TC) triggered by alcohol withdrawal.

Takotsubo Cardiomyopathy figure 2
Coronary angiography during left-heart cathertization showing normal epicardial coronary arteries.

Takotsubo Cardiomyopathy figure 3
Left ventriculogram, end-systolic phase; the extensive area around the apex shows akinesis, and the basal segments display hypercontraction.


Outcome of the case. The patient was transferred to the intensive care unit for management of alcohol withdrawal with delirium with intravenous fluids, benzodiazepines, and vitamins. He eventually made a full recovery and was discharged, with clinic follow-up visits arranged.

Discussion. TC is also called stress cardiomyopathy, apical ballooning syndrome, and broken heart syndrome. Initially described in the 1990s in Japan, this reversible cardiomyopathy is characterized by a distinctive shape observed on left ventriculography, described as apical ballooning. This shape is similar to a Japanese takotsubo pot, which has a narrow neck and a round bottom and is used by fishermen to trap octopus.1

TC is characterized by transient regional systolic dysfunction of the LV, mimicking myocardial infarction (MI), but in the absence of angiographic evidence of obstructive coronary artery disease. Patients with TC can present with features seen in acute MI, including chest discomfort, ECG abnormalities (eg, ST-segment elevation, abnormal Q waves, T-wave inversion), dysrhythmia, and shock.2 Based on the results of recent analyses reported from several countries, this condition probably accounts for approximately 1% to 2% of all cases of suspected acute MI.3-5

Pathophysiology. The exact physiopathology of TC has not been fully elucidated. There likely is a strong interplay between the autonomic, neurologic, and cardiovascular systems.6 Several theories have been proposed to explain the transient cardiac dysfunction in TC, of which the most accepted is a catecholamine surge triggered by emotional or physical stressors7—including those related to alcohol withdrawal. TC is much more common in postmenopausal women (more than 90% of cases), and reduced estrogen levels could play a role in the pathogenesis by predisposing endothelial cells to sympathetic myocardial stunning.8

Alcohol withdrawal is a period of hyperadrenergic state, with high levels of plasma catecholamines during the first days of detoxification, associated with an increase of β-adrenergic receptor sensitivity.9-11 Epinephrine and norepinephrine have been reported to be markedly elevated in patients with TC, which may contribute to myocardial stunning. In addition, elevated levels of plasma catecholamines may cause coronary macrocirculation and microcirculation vasospasms.6 Catecholamines may exert a direct toxic effect on the myocardium through changes in autonomic tone, enhanced lipid mobility, calcium overload, free radical production, or increased sarcolemmal permeability.1

The different morphologic LV variants of TC could be explained by the different distribution of adrenergic receptors.6 Differences in the density of β-adrenergic receptors in the apex and base of the heart can account for the unusual apical ballooning.1 However, not all cases of TC involve strictly the apical segment of the LV. Patterns of LV motion abnormality include the apical type, and atypical variants including midventricular, basal, focal (limited to an isolated segment), and global types.

Patients with TC often have elevated levels of cardiac biomarkers with only mildly elevated troponin I levels. There are no generally accepted cutoff points for troponin I elevation that ultimately would influence clinical management.6

One possible explanation for our patient’s initial loss of consciousness is a transient arrhythmia (especially given his history of atrial fibrillation). Recent murine studies have shown that the risk of fatal arrhythmias increases during alcohol withdrawal due to sympathetic predominance.12,13 Although a seizure could be another possible explanation, his normal head CT and EEG results make this less likely.

Diagnosis. No consensus exists on the diagnostic criteria for TC. Researchers at the Mayo Clinic proposed diagnostic criteria in 200414: (1) transient hypokinesis, akinesis, or dyskinesis in LV midsegments with or without apical involvement; regional wall motion abnormalities extending beyond a single epicardial vascular distribution; and, frequently but not always, a stressful trigger; (2) the absence of obstructive coronary artery disease or angiographic evidence of acute plaque rupture; (3) new ECG abnormalities (ST-segment elevation and/or T-wave inversion) or modest elevation of cardiac troponin; and (4) the absence of pheochromocytoma and myocarditis.15

Treatment and prognosis. No guidelines are available for the treatment of TC, and decisions must be individualized. Since sympathetic activation is thought to contribute to the pathogenesis, it is reasonable to consider long-term β-blockade with the goal of preventing recurrence. Some data suggest that the risk of recurrence in the first few years after the initial episode ranges from 2% to 10%.6 Recurrence rates may be lower in patients maintained on comprehensive β-blockade.6

The prognosis of patients with TC is generally favorable. Recovery of LV function occurs over a period of days to weeks with appropriate medical therapy.1

The paucity of reported cases of TC triggered by alcohol withdrawal may be related to a lack of routine evaluation of cardiac ischemia. TC should be included among the differential diagnoses in patients with alcohol withdrawal or delirium tremens who also have chest pain. Of course, acutely intoxicated patients present a very significant challenge to accurate and timely diagnosis. The fact that severe alcohol withdrawal can be a precursor of TC underscores the importance of adequate care of these patients to minimize adrenergic surge.


  1. Hare JM. The dilated, restrictive, and infiltrative cardiomyopathies. In: Bonow RO, Mann DL, Zipes DP, Libby P, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. Vol 1. 9th ed. Philadelphia, PA: Elsevier Saunders; 2012:1561-1581.
  2. Tsuchihashi K, Ueshima K, Uchida T, et al; Angina Pectoris-Myocardial Infarction Investigations in Japan. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol. 2001;38(1):11-18.
  3. Kurowski V, Kaiser A, von Hof K, et al. Apical and midventricular transient left ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): frequency, mechanisms, and prognosis. Chest. 2007;132(3):809-816.
  4. Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J. 2006;27(13):1523-1529.
  5. Prasad A, Dangas G, Srinivasan M, et al. Incidence and angiographic characteristics of patients with apical ballooning syndrome (takotsubo/stress cardiomyopathy) in the HORIZONS-AMI trial: an analysis from a multicenter, international study of ST-elevation myocardial infarction. Catheter Cardiovasc Interv. 2014;83(3):343-348.
  6. Veillet-Chowdhury M, Hassan SF, Stergiopoulos K. Takotsubo cardiomyopathy: a review. Acute Card Care. 2014;16(1):15-22.
  7. Linnoila M, Mefford I, Nutt D, Adinoff B. Alcohol withdrawal and noradrenergic function. Ann Intern Med. 1987;107(6):875-889.
  8. Wittstein IS, Thiemann DR, Lima JAC, et al. Neurohormonal features of myocardial stunning due to sudden emotional stress. N Engl J Med. 2005;​352(6):539-548.
  9. Kupari M, Koskinen P. Alcohol, cardiac arrhythmias and sudden death. In: Chadwick DJ, Goode JA, eds. Novartis Foundation Symposium 216—Alcohol and Cardiovascular Diseases. Chichester, England: John Wiley & Sons; 2007:68-85.
  10. Denison H, Jern S, Jagenburg R, Wendestam C, Wallerstedt S. Influence of increased adrenergic activity and magnesium depletion on cardiac rhythm in alcohol withdrawal. Br Heart J. 1994;72(6):554-560.
  11. Banerjee SP, Sharma VK, Khanna JM. Alterations in β-adrenergic receptor binding during ethanol withdrawal. Nature. 1978;276(5686):407-409.
  12. Shirafuji S, Liu J, Okamura N, Hamada K, Fujimiya T. QT interval dispersion and cardiac sympathovagal balance shift in rats with acute ethanol withdrawal. Alcohol Clin Exp Res. 2010;34(2):223-230.
  13. Liu J, Shirafuji S, Fujimiya T. Rats in acute withdrawal from ethanol exhibit left ventricular systolic dysfunction and cardiac sympathovagal balance shift. Alcohol. 2009;43(3):207-216.
  14. Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (tako-tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J. 2008;155(3):408-417.
  15. Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation. 2008;118(25):​2754-2762.