Neurohumoral Features of Myocardial Stunning Due to Sudden Emotional Stress
Ilan S. Wittstein, M.D., David R. Thiemann, M.D., Joao A.C. Lima, M.D., Kenneth L. Baughman, M.D., Steven P. Schulman, M.D., Gary Gerstenblith, M.D., Katherine C. Wu, M.D., Jeffrey J. Rade, M.D., Trinity J. Bivalacqua, M.D., Ph.D., and Hunter C. Champion, M.D., Ph.D.
Background Reversible left ventricular dysfunction precipitatedby emotional stress has been reported, but the mechanism remainsunknown.
Methods We evaluated 19 patients who presented with left ventriculardysfunction after sudden emotional stress. All patients underwentcoronary angiography and serial echocardiography; five underwentendomyocardial biopsy. Plasma catecholamine levels in 13 patientswith stress-related myocardial dysfunction were compared withthose in 7 patients with Killip class III myocardial infarction.
Results The median age of patients with stress-induced cardiomyopathywas 63 years, and 95 percent were women. Clinical presentationsincluded chest pain, pulmonary edema, and cardiogenic shock.Diffuse T-wave inversion and a prolonged QT interval occurredin most patients. Seventeen patients had mildly elevated serumtroponin I levels, but only 1 of 19 had angiographic evidenceof clinically significant coronary disease. Severe left ventriculardysfunction was present on admission (median ejection fraction,0.20; interquartile range, 0.15 to 0.30) and rapidly resolvedin all patients (ejection fraction at two to four weeks, 0.60;interquartile range, 0.55 to 0.65; P<0.001). Endomyocardialbiopsy showed mononuclear infiltrates and contraction-band necrosis.Plasma catecholamine levels at presentation were markedly higheramong patients with stress-induced cardiomyopathy than amongthose with Killip class III myocardial infarction (median epinephrinelevel, 1264 pg per milliliter [interquartile range, 916 to 1374]vs. 376 pg per milliliter [interquartile range, 275 to 476];norepinephrine level, 2284 pg per milliliter [interquartilerange, 1709 to 2910] vs. 1100 pg per milliliter [interquartilerange, 914 to 1320]; and dopamine level, 111 pg per milliliter[interquartile range, 106 to 146] vs. 61 pg per milliliter [interquartilerange, 46 to 77]; P<0.005 for all comparisons).
Conclusions Emotional stress can precipitate severe, reversibleleft ventricular dysfunction in patients without coronary disease.Exaggerated sympathetic stimulation is probably central to thecause of this syndrome.
The potentially lethal consequences of emotional stress aredeeply rooted in folk wisdom, as reflected by phrases such as"scared to death" and "a broken heart." In the past decade,cardiac contractile abnormalities and heart failure have beenreported after acute emotional stress,1,2,3,4,5,6 but the mechanismremains unknown. We evaluated 19 patients with "stress cardiomyopathy,"a syndrome of profound myocardial stunning precipitated by acuteemotional stress, in an effort to identify the clinical featuresthat distinguish this syndrome from acute myocardial infarctionand the cause of transient stress-induced myocardial dysfunction.
Methods
Study Patients
Nineteen previously healthy patients were admitted to the coronarycare unit at Johns Hopkins Hospital or Johns Hopkins BayviewMedical Center in Baltimore with chest pain or symptomatic heartfailure precipitated by acute emotional stress. Patients wereevaluated by means of serial electrocardiography and serialmeasurement of cardiac isoenzymes, including creatine kinase,creatine kinase MB fraction, and troponin I. All 19 patientsunderwent coronary angiography; 16 also underwent concomitantleft ventriculography. Five patients underwent right-heart catheterizationand endomyocardial biopsy, and five underwent contrast-enhancedcardiac magnetic resonance imaging (MRI) to identify myocardialnecrosis. All patients underwent two-dimensional transthoracicechocardiography within 24 hours after the onset of symptomsand again on hospital day 3, 4, 5, 6, or 7 (median, day 4);17 patients underwent outpatient echocardiography a median of21 days after presentation. Wall-motion abnormalities on echocardiographywere assessed by means of a standard 16-segment model,7 withnumerical scoring of contractile function (a score of 1 indicatesnormal contraction, a score of 2 mild hypokinesis, a score of3 severe hypokinesis, a score of 4 akinesis, and a score of5 dyskinesis).
Neurohumoral Assessment
Plasma levels of catecholamines, metabolites, and neuropeptideswere measured on hospital day 1 or 2; day 3, 4, or 5; and day7, 8, or 9 in 13 patients with stress cardiomyopathy and a conveniencesample of 7 female patients hospitalized with Killip class IIImyocardial infarction. The latter patients were chosen for comparisonbecause they had similar clinical presentations and were expectedto have high sympathetic tone. Patients remained supine forat least 60 minutes before undergoing phlebotomy. Blood sampleswere placed on ice and immediately centrifuged, and the plasmawas flash-frozen. Plasma levels of catecholamines and theirmetabolites were measured by high-performance liquid chromatography8;brain natriuretic peptide and neuropeptide Y were measured byenzyme immunoassay or radioimmunoassay.9,10
Statistical Analysis
Continuous variables are presented as medians and interquartileranges; ordinal variables are presented as means ±SD.The MannWhitney test (SAS software, version 8.0; SASInstitute) was used to compare plasma catecholamine levels inpatients with stress cardiomyopathy with those in patients withKillip class III myocardial infarction. For plasma catecholaminelevels, P values of less than 0.005 remained significant afterBonferroni correction for multiple comparisons. The Wilcoxonsigned-rank test was used to compare ejection fractions andechocardiographic scores at various times in the group of patientswith stress cardiomyopathy. A two-tailed P value of less than0.05 was considered to indicate statistical significance.
The study was conducted between November 1999 and September2003. All authors participated in data collection. Oral informedconsent was obtained from all patients, and the protocol wasapproved by the institutional review board of Johns HopkinsUniversity School of Medicine.
Results
Clinical Characteristics
The median age of patients with stress cardiomyopathy was 63years (interquartile range, 52 to 71). Eighteen patients (95percent) were women, of whom all but two were postmenopausal(Table 1). News of an unexpected death precipitated cardiacdysfunction in about half the patients. The remainder experienceda variety of causes of emotional stress (Table 1). All patientshad severe chest pain, dyspnea, or both during emotional stressand presented to the emergency department a median of two hours(interquartile range, one to five) after the onset of symptoms.Three patients required intraaortic balloon counterpulsationfor hemodynamic support, and one patient had ventricular fibrillation.
Table 1. Clinical Characteristics of 19 Patients with Stress Cardiomyopathy on Admission.
Electrocardiography
The initial electrocardiogram showed sinus rhythm in all patientswith stress cardiomyopathy, with a median heart rate of 85 beatsper minute. Five patients (26 percent) had a prolonged PR interval,and five (26 percent) had a prolonged QT interval correctedfor heart rate (QTc). Two patients (11 percent) had ST-segmentelevation of at least 1 mm, and three patients (16 percent)had diffuse T-wave inversion. Pathologic Q waves were seen inleads V1, V2, and V3 in seven patients (37 percent) and in leadaVL in five (26 percent). Within 48 hours after the onset ofsymptoms, all 19 patients had marked prolongation of the QTinterval (median QTc, 542 msec; interquartile range, 490 to592) and all but 1 had deep, symmetric, T-wave inversion (Figure 1).In most patients, the QTc normalized within one or two days,whereas the T-wave inversion resolved more slowly and oftenonly partially. Pathologic precordial Q waves typically resolvedbefore hospital discharge, with restoration of normal R-waveprogression.
Figure 1. Typical Electrocardiograms Obtained 24 to 48 Hours after Presentation in Four Patients with Stress Cardiomyopathy.
Marked prolongation of the QT interval and diffuse symmetric T-wave inversion are present in all four electrocardiograms. Loss of R-wave progression in leads V1, V2, and V3 is also evident in Panels C and D.
Cardiac Enzymes
Peak troponin I levels were only mildly elevated, with a medianvalue of 0.18 ng per milliliter (interquartile range, 0.08 to0.69; normal value, <0.06). Troponin I was undetectable intwo patients. The peak creatine kinase level was 133 IU perliter (interquartile range, 114 to 273; normal value, <170),and the peak creatine kinase MB level was 10 ng per milliliter(interquartile range, 5 to 14; normal value, <7).
Echocardiography
The median left ventricular ejection fraction on the initialechocardiogram (hospital day 1) was 0.20 (interquartile range,0.15 to 0.30) (Figure 2). All patients had a similar contractilepattern, with preserved basal function, moderate-to-severe dysfunctionin the midventricle, and apical akinesis or dyskinesis (meanechocardiographic scores, 1.2±0.2, 3.2±0.5, and3.7±0.5, respectively). By hospital day 3, 4, 5, 6, or7 (a median of four days after presentation), the left ventricularejection fraction had improved to 0.45 and the midventricularand apical segments were only mildly hypokinetic, with echocardiographicscores of 1.0±0.0 at the base, 1.9±0.7 at themidventricle, and 2.3±1.2 at the apex. At outpatientfollow-up (a median of 21 days after presentation), the leftventricular ejection fraction was 0.60 (interquartile range,0.55 to 0.65; P<0.001 for the comparison with values at presentationand during inpatient follow-up), and all segments had normalcontractility.
Figure 2. Serial Echocardiographic Assessment of the Ejection Fraction in 19 Patients with Stress Cardiomyopathy.
Echocardiography was performed on admission; on hospital day 3, 4, 5, 6, or 7 (median, day 4); and at outpatient follow-up (a median of 21 days after the onset of symptoms). Gray lines illustrate values for individual patients. The black bar represents the median ejection fraction at each time; error bars show the interquartile range. P<0.001 for the comparison between admission and inpatient values, and P<0.001 for the comparisons between admission and outpatient values and between inpatient and outpatient values.
Magnetic Resonance Imaging
In the five patients who underwent cardiac MRI, cine studiesconfirmed the pattern and degree of left ventricular dysfunctionseen on echocardiography. None of the patients had evidenceof myocardial necrosis on contrast-enhanced imaging (Figure 3C).
Figure 3. Ventriculographic Assessment of Cardiac Function and MRI Assessment of Myocardial Viability at Admission in a Patient with Stress Cardiomyopathy.
Contrast-enhanced ventriculography during diastole, in Panel A, and systole, in Panel B, demonstrates apical and midventricular akinesis, with relative sparing of the base of the heart (arrow). In Panel C, MRI in the long-axis view reveals that the akinetic regions seen on ventriculography are dark and hypoenhanced, consistent with the presence of viable myocardium. Panel D, which is presented for purposes of comparison, shows hyperenhancement (arrow), indicative of necrosis and decreased viability, after an acute anterior myocardial infarction.
Cardiac Catheterization
Thirteen patients underwent emergency angiography on admission,and six underwent angiography on hospital day 3, 4, 5, or 6.Eighteen patients (95 percent) had normal coronary arteriesor mild luminal irregularities; one patient had a luminal narrowingof 70 percent in the proximal left anterior descending coronaryartery. No patient had angiographic evidence of epicardial spasm.Patients undergoing catheterization on hospital day 1 had amedian left ventricular end-diastolic pressure of 30 mm Hg (interquartilerange, 25 to 31). Contrast-enhanced left ventriculography revealedapical and midventricular akinesis or dyskinesis with normalcontractility of the base (Figure 3A and Figure 3B) and an ejectionfraction of 0.25 (interquartile range, 0.15 to 0.30). Patientsundergoing ventriculography on day 3, 4, 5, or 6 had a significantimprovement in the left ventricular end-diastolic pressure (median,16 mm Hg; interquartile range, 15 to 24; P=0.005) and the ejectionfraction (0.43; interquartile range, 0.40 to 0.50; P=0.007),as compared with values on day 1.
Endomyocardial Biopsy
Of the five patients who underwent endomyocardial biopsy, fourhad interstitial infiltrates consisting primarily of mononuclearlymphocytes and macrophages and contraction bands without myocytenecrosis. The other patient had an extensive inflammatory lymphocyticinfiltrate and multiple foci of contraction-band myocyte necrosis.
Plasma Catecholamines and Neuropeptides
All subgroups had similar demographic characteristics. The medianage was 66 years among the 13 patients who underwent neurohumoralassessment, 63 years among the 6 patients who did not undergoneurohumoral assessment, and 60 years among the 7 control patientswith myocardial infarction. On hospital day 1 or 2, plasma levelsof catecholamines (i.e., epinephrine, norepinephrine, and dopamine)among patients with stress cardiomyopathy were 2 to 3 timesthe values among patients with Killip class III myocardial infarctionand 7 to 34 times published normal values11 (Table 2). Initiallevels of plasma dihydroxyphenylalanine, dihydroxyphenylglycol,and dihydroxyphenylacetic acid among patients with stress cardiomyopathywere approximately two times the values among patients withmyocardial infarction and two to three times normal values,consistent with the presence of enhanced catecholamine synthesis,neuronal reuptake, and neuronal metabolism, respectively.
Table 2. Plasma Catecholamine and Neuropeptide Levels.
Plasma levels of metanephrine and normetanephrine, which areextraneuronal catecholamine metabolites, were also proportionatelyincreased among patients with stress cardiomyopathy. Plasmalevels of neuropeptide Y, which is stored with catecholaminesin postganglionic sympathetic nerves and adrenal chromaffincells and released during stress, were markedly increased amongpatients with stress cardiomyopathy, as were plasma levels ofbrain natriuretic peptide and serotonin.
By hospital day 7, 8, or 9, plasma levels of most catecholamines,neuronal metabolites, and neuropeptides in patients with stresscardiomyopathy were one third to one half of the peak valuesbut remained substantially higher than those in patients withmyocardial infarction. In contrast, plasma brain natriureticpeptide levels declined rapidly in the patients with stresscardiomyopathy (correlating with rapidly improving left ventricularsystolic function) and by day 7, 8, or 9 were lower than thosein patients with myocardial infarction.
Discussion
There have been several reports of patients with profound, reversibleleft ventricular dysfunction after sudden emotional stress.1,2,3,4,5,6Some reports are from Japan, where the pattern of left ventriculardysfunction has been referred to as "takotsubo cardiomyopathy,"6named for the fishing pot with a narrow neck and wide base thatis used to trap octopus. More recently, the term "transientleft ventricular apical ballooning" has been used to describesimilar cardiac contractile abnormalities in patients afteremotional or physical stress.5,14 Despite the increasing awarenessof acute stress-induced myocardial dysfunction, the mechanismremains unknown.
Our patients with stress cardiomyopathy had supraphysiologiclevels of plasma catecholamines and stress-related neuropeptides.Initial plasma levels were several times those of patients withmyocardial infarction and remained markedly elevated even aweek after the onset of symptoms. Our data suggest the activationof the adrenomedullary hormonal system, with marked elevationin plasma epinephrine and metanephrine levels. Enhanced sympathoneuralactivity is also suggested by the increased plasma levels ofdihydroxyphenylalanine, dihydroxyphenylglycol, norepinephrine,and normetanephrine, reflecting increased synthesis of norepinephrine,neuronal reuptake and metabolism, spillover, and extraneuronalmetabolism, respectively.
The mechanism underlying the association between sympatheticstimulation and myocardial stunning is unknown. One possibilityis ischemia resulting from epicardial coronary arterial spasm.Increased sympathetic tone from mental stress can cause vasoconstrictionin patients without coronary disease.15 In an angiographic studyof patients with takotsubo cardiomyopathy, 70 percent had coronaryspasm in response to provocative maneuvers, and electrocardiographicevidence of ST-segment elevation was common at presentation.6Our patients, however, had no angiographic evidence of epicardialspasm, and ST-segment elevation was rarely seen. The patientsdid initially have contractile abnormalities in multiple vascularterritories, but multivessel epicardial spasm as an explanationfor this finding seems unlikely, given the relative absenceof ST-segment elevation and minimal enzymatic evidence of myocardialnecrosis.
An alternative mechanism is microvascular spasm. Abnormal coronaryflow in the absence of obstructive disease has recently beenreported in patients with stress-related myocardial dysfunction.16Others have demonstrated reduced coronary-flow reserve and regionaldefects on cardiac [123I]metaiodobenzyl-guanidineenhancedimaging in such patients,17 suggesting the presence of sympatheticallymediated microcirculatory dysfunction.
A third possible mechanism of catecholamine-mediated myocardialstunning is direct myocyte injury. Elevated catecholamine levelsdecrease the viability of myocytes through cyclic AMPmediatedcalcium overload.18 Catecholamines are also a potential sourceof oxygen-derived free radicals and, in animal models, causemyocyte injury that is attenuated by antioxidants.19 Free radicalscan interfere with sodium and calcium transporters, possiblyresulting in myocyte dysfunction through increased transsarcolemmalcalcium influx and cellular calcium overload.20 Histologically,catecholamines have been associated with contraction-band necrosis,a unique form of myocyte injury characterized by hypercontractedsarcomeres, dense eosinophilic transverse bands, and an interstitialmononuclear inflammatory response that is distinct from thepolymorphonuclear inflammation seen with infarction. Contraction-bandnecrosis has been described in clinical states of catecholamineexcess such as pheochromocytoma21 and subarachnoid hemorrhage.22It has also been observed post mortem in people who died underterrifying circumstances such as fatal asthma23 and violentassault,24 suggesting that catecholamines may be an importantlink between emotional stress and cardiac injury. The biopsyfindings in our patients are consistent with the presence ofan elevated catecholamine state: four of five patients had mononuclearinflammatory infiltrates, while the fifth had extensive contraction-bandnecrosis.
In earlier reports5,6,14 and in our series, stress-related myocardialstunning was characterized by contractile abnormalities of theapex and midportion of the left ventricle with relative sparingof the basal segments (Figure 3A and Figure 3B). The reasonfor this distinctive contractile pattern is unknown. Local releaseof catecholamines from cardiac sympathetic efferent neuronsis an unlikely explanation, given the higher norepinephrinecontent25 and greater density of sympathetic nerves26 at thebase of the heart than in the apex. There is evidence that apicalmyocardium has enhanced responsiveness to sympathetic stimulation,27potentially making the apex more vulnerable to sudden surgesin circulating catecholamine levels. Alternatively, a base-to-apexperfusion gradient, similar to that described in patients withcoronary risk factors,28 could result in regional differencesin myocardial blood flow in the setting of catecholamine-mediatedepicardial or microvascular vasoconstriction.
Although the striking preponderance of women in our study andin other reports5,6,14,16 suggests a biologic susceptibilityto stress-related myocardial dysfunction, the basis of thispredisposition is unknown. Sex hormones exert important influenceson the sympathetic neurohormonal axis29 as well as on coronaryvasoreactivity,30 but sex-related differences in catecholaminemetabolism and responsiveness are complex and remain poorlyunderstood. Men have higher levels of basal sympathetic activitythan women,29 produce higher levels of plasma catecholaminesin response to emotional stress,31 and are more sensitive tocatecholamine-mediated vasoconstriction.32 However, women appearto be more vulnerable to sympathetically mediated myocardialstunning, as evidenced by increased catecholamine production33and transient left ventricular dysfunction34 after subarachnoidhemorrhage.
Although the incidence of stress cardiomyopathy is unknown,it is likely to be more common than generally thought. Thoughwe reported on only patients with emotional sources of stress,we have observed identical presentations in patients after awide variety of neurologic injuries (unpublished data); othershave previously reported a similar pattern of transient myocardialdysfunction in patients after numerous types of nonemotionalstress.5,6,14,35 The overlapping clinical features in all thesepresentations suggest that myocardial stunning resulting fromemotional stress may share a common mechanism with "neurogenicstunned myocardium," which has been described after subarachnoidhemorrhage36 and stroke37 and which is believed to be mediatedby catecholamines.
Because patients with stress cardiomyopathy typically presentwith clinical features resembling those of acute myocardialinfarction, coronary angiography is indicated in most cases.In the absence of critical coronary arterial disease, the diagnosisof stress cardiomyopathy should be considered when the historytaking reveals that cardiac symptoms were precipitated by intenseemotional stress, when there is a unique pattern of left ventriculardysfunction characterized by apical and midventricular contractileabnormalities with sparing of the basal segments, and when thereis minimal elevation of cardiac enzymes despite the presenceof large regions of focal akinesis in the myocardium. The clinicaldiagnosis is reinforced by the development of a markedly prolongedQT interval with deep precordial or global T-wave inversionon electrocardiography during the first 48 hours in the hospital,as well as rapidly improving cardiac contractility on serialechocardiography.
The treatment of stress cardiomyopathy, beyond standard supportivecare for congestive heart failure with diuretics and vasodilators,remains largely empirical. Because our data implicate massivecatecholamine release in stress-induced myocardial stunning,we avoid using pressors and beta-agonists whenever possibleand instead rely on mechanical circulatory support in patientswith severe hemodynamic compromise. When medical support isprovided initially, patients with stress cardiomyopathy haverapid clinical and echocardiographic improvement and have anexcellent prognosis. In the four years that we have followedthese patients, none have died, had a recurrence, or had a declinein left ventricular function. This outcome accords with thefavorable prognosis that has been previously reported.5
Our study has the inherent limitations of any small, observationalcase series. Although the age and sex of the seven control patientswith Killip class III myocardial infarction were similar tothose of our patients with stress cardiomyopathy, they werenot selected by means of systematic random sampling, and thus,selection bias is possible, albeit unlikely. In addition, althoughour data show an intriguing association between sympatheticactivation and stress cardiomyopathy, they do not prove a causalrelationship. Elevated plasma catecholamine levels may be anepiphenomenon or a secondary response in patients with stresscardiomyopathy, rather than the root cause.
In conclusion, a unique pattern of transient myocardial dysfunctioncan occur after severe emotional stress. Patients with thissyndrome have evidence of exaggerated sympathetic activation,with plasma catecholamine levels several times those in age-and sex-matched patients with Killip class III myocardial infarction.Although our data suggest that catecholamines may be centralto the mechanism of stress-related myocardial stunning, a morecomplete understanding of the pathogenesis of this syndromeawaits further research.
Supported in part by the Bernard A. and Rebecca S. Bernard Foundation.Drs. Thiemann, Lima, Schulman, Gerstenblith, and Wu were supportedin part by the Donald W. Reynolds Foundation.
Source Information
From the Division of Cardiology, Department of Medicine (I.S.W., D.R.T., J.A.C.L., S.P.S., G.G., K.C.W., J.J.R., H.C.C.), and the Brady Urological Institute (T.J.B.), Johns Hopkins University School of Medicine, Baltimore; the Department of Epidemiology, Johns Hopkins University School of Public Health, Baltimore (D.R.T.); and the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston (K.L.B.).
Address reprint requests to Dr. Wittstein at the Division of Cardiology, Johns Hopkins Hospital, Carnegie 568, 600 N. Wolfe St., Baltimore, MD 21287, or at iwittste{at}jhmi.edu.
References
Pavin D, Le Breton H, Daubert C. Human stress cardiomyopathy mimicking acute myocardial syndrome. Heart 1997;78:509-511. [Free Full Text]
Kawai S, Suzuki H, Yamaguchi H, et al. Ampulla cardiomyopathy (`Takotsubo' cardiomyopathy) -- reversible left ventricular dysfunction: with ST segment elevation. Jpn Circ J 2000;64:156-159. [Erratum, Jpn Circ J 2000;64:237.] [CrossRef][Medline]
Villareal RP, Achari A, Wilansky S, Wilson JM. Anteroapical stunning and left ventricular outflow tract obstruction. Mayo Clin Proc 2001;76:79-83. [Abstract]
Brandspiegel HZ, Marinchak RA, Rials SJ, Kowey PR. A broken heart. Circulation 1998;98:1349-1349. [Free Full Text]
Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol 2001;38:11-18. [Free Full Text]
Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448-455. [CrossRef][Web of Science][Medline]
Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography: American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:358-367. [Medline]
Grouzmann E, Fathi M, Gillet M, et al. Disappearance rate of catecholamines, total metanephrines, and neuropeptide Y from the plasma of patients after resection of pheochromocytoma. Clin Chem 2001;47:1075-1082. [Erratum, Clin Chem 2001;47:1748.] [Free Full Text]
Jonsson BH, Hellstrom PM. Motilin- and neuropeptide Y-like immunoreactivity in a psychophysiological stress experiment on patients with functional dyspepsia. Integr Physiol Behav Sci 2000;35:256-265. [CrossRef][Web of Science][Medline]
Onuoha GN, Nugent AM, Hunter SJ, et al. Neuropeptide variability in man. Eur J Clin Invest 2000;30:570-577. [CrossRef][Web of Science][Medline]
Goldstein DS, Eisenhofer G, Kopin IJ. Sources and significance of plasma levels of catechols and their metabolites in humans. J Pharmacol Exp Ther 2003;305:800-811. [Free Full Text]
Redfield MM, Rodeheffer RJ, Jacobsen SJ, Mahoney DW, Bailey KR, Burnett JC Jr. Plasma brain natriuretic peptide concentration: impact of age and gender. J Am Coll Cardiol 2002;40:976-982. [Free Full Text]
Spreux-Varoquaux O, Alvarez JC, Berlin I, et al. Differential abnormalities in plasma 5-HIAA and platelet serotonin concentrations in violent suicide attempters: relationships with impulsivity and depression. Life Sci 2001;69:647-657. [CrossRef][Web of Science][Medline]
Desmet WJ, Adriaenssens BF, Dens JA. Apical ballooning of the left ventricle: first series in white patients. Heart 2003;89:1027-1031. [Free Full Text]
Lacy CR, Contrada RJ, Robbins ML, et al. Coronary vasoconstriction induced by mental stress (simulated public speaking). Am J Cardiol 1995;75:503-505. [CrossRef][Web of Science][Medline]
Bybee KA, Prasad A, Barsness GW, et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol 2004;94:343-346. [CrossRef][Web of Science][Medline]
Sadamatsu K, Tashiro H, Maehira N, Yamamoto K. Coronary microvascular abnormality in the reversible systolic dysfunction observed after noncardiac disease. Jpn Circ J 2000;64:789-792. [CrossRef][Medline]
Mann DL, Kent RL, Parsons B, Cooper G. Adrenergic effects on the biology of the adult mammalian cardiocyte. Circulation 1992;85:790-804. [Free Full Text]
Singal PK, Kapur N, Dhillon KS, Beamish RE, Dhalla NS. Role of free radicals in catecholamine-induced cardiomyopathy. Can J Physiol Pharmacol 1982;60:1390-1397. [Web of Science][Medline]
Bolli R, Marban E. Molecular and cellular mechanisms of myocardial stunning. Physiol Rev 1999;79:609-634. [Free Full Text]
Wilkenfeld C, Cohen M, Lansman SL, et al. Heart transplantation for end-stage cardiomyopathy caused by an occult pheochromocytoma. J Heart Lung Transplant 1992;11:363-366. [Web of Science][Medline]
Neil-Dwyer G, Walter P, Cruickshank JM, Doshi B, O'Gorman P. Effect of propranolol and phentolamine on myocardial necrosis after subarachnoid haemorrhage. Br Med J 1978;2:990-992. [Free Full Text]
Drislane FW, Samuels MA, Kozakewich H, Schoen FJ, Strunk RC. Myocardial contraction band lesions in patients with fatal asthma: possible neurocardiologic mechanisms. Am Rev Respir Dis 1987;135:498-501. [Web of Science][Medline]
Cebelin MS, Hirsch CS. Human stress cardiomyopathy: myocardial lesions in victims of homicidal assaults without internal injuries. Hum Pathol 1980;11:123-132. [Web of Science][Medline]
Pierpont GL, DeMaster EG, Cohn JN. Regional differences in adrenergic function within the left ventricle. Am J Physiol 1984;246:H824-H829. [Web of Science][Medline]
Kawano H, Okada R, Yano K. Histological study on the distribution of autonomic nerves in the human heart. Heart Vessels 2003;18:32-39. [CrossRef][Web of Science][Medline]
Mori H, Ishikawa S, Kojima S, et al. Increased responsiveness of left ventricular apical myocardium to adrenergic stimuli. Cardiovasc Res 1993;27:192-198. [Free Full Text]
Hernandez-Pampaloni M, Keng FY, Kudo T, Sayre JS, Schelbert HR. Abnormal longitudinal, base-to-apex myocardial perfusion gradient by quantitative blood flow measurements in patients with coronary risk factors. Circulation 2001;104:527-532. [Free Full Text]
Hinojosa-Laborde C, Chapa I, Lange D, Haywood JR. Gender differences in sympathetic nervous system regulation. Clin Exp Pharmacol Physiol 1999;26:122-126. [CrossRef][Web of Science][Medline]
Sader MA, Celermajer DS. Endothelial function, vascular reactivity and gender differences in the cardiovascular system. Cardiovasc Res 2002;53:597-604. [Free Full Text]
Frankenhaeuser M, Dunne E, Lundberg U. Sex differences in sympathetic-adrenal medullary reactions induced by different stressors. Psychopharmacology (Berl) 1976;47:1-5. [CrossRef][Medline]
Kneale BJ, Chowienczyk PJ, Brett SE, Coltart DJ, Ritter JM. Gender differences in sensitivity to adrenergic agonists of forearm resistance vasculature. J Am Coll Cardiol 2000;36:1233-1238. [Free Full Text]
Lambert G, Naredi S, Eden E, Rydenhag B, Friberg P. Monoamine metabolism and sympathetic nervous activation following subarachnoid haemorrhage: influence of gender and hydrocephalus. Brain Res Bull 2002;58:77-82. [CrossRef][Web of Science][Medline]
Mayer SA, Lin J, Homma S, et al. Myocardial injury and left ventricular performance after subarachnoid hemorrhage. Stroke 1999;30:780-786. [Free Full Text]
Sharkey SW, Shear W, Hodges M, Herzog CA. Reversible myocardial contraction abnormalities in patients with an acute noncardiac illness. Chest 1998;114:98-105. [Free Full Text]
Kono T, Morita H, Kuroiwa T, Onaka H, Takatsuka H, Fujiwara A. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol 1994;24:636-640. [Abstract]
Triposkiadis, F., Karayannis, G., Giamouzis, G., Skoularigis, J., Louridas, G., Butler, J.
(2009). The sympathetic nervous system in heart failure physiology, pathophysiology, and clinical implications.. J Am Coll Cardiol
54: 1747-1762
[Abstract][Full Text]
Agarwal, S., Lyon, A., Nachev, P., Everitt, A.
(2009). The nervous heart: a case report and discussion of an under-recognized clinical problem. QJM
102: 807-809
[Full Text]
Griffin, S., Logue, B.
(2009). Takotsubo Cardiomyopathy: A Nurse's Guide. Crit Care Nurse
29: 32-42
[Full Text]
Tsai, T. T., Nallamothu, B. K., Prasad, A., Saint, S., Bates, E. R.
(2009). A Change of Heart. NEJM
361: 1010-1016
[Full Text]
Nef, H. M., Mollmann, H., Troidl, C., Kostin, S., Voss, S., Hilpert, P., Behrens, C. B., Rolf, A., Rixe, J., Weber, M., Hamm, C. W., Elsasser, A.
(2009). Abnormalities in intracellular Ca2+ regulation contribute to the pathomechanism of Tako-Tsubo cardiomyopathy. Eur Heart J
30: 2155-2164
[Abstract][Full Text]
Dunser, M. W., Hasibeder, W. R.
(2009). Sympathetic Overstimulation During Critical Illness: Adverse Effects of Adrenergic Stress. J Intensive Care Med
24: 293-316
[Abstract]
Madhavan, M, Borlaug, B A, Lerman, A, Rihal, C S, Prasad, A
(2009). Stress hormone and circulating biomarker profile of apical ballooning syndrome (Takotsubo cardiomyopathy): insights into the clinical significance of B-type natriuretic peptide and troponin levels. Heart
95: 1436-1441
[Abstract][Full Text]
Barletta, G., Del Pace, S., Boddi, M., Del Bene, R., Salvadori, C., Bellandi, B., Coppo, M., Saletti, E., Gensini, G. F.
(2009). Abnormal coronary reserve and left ventricular wall motion during cold pressor test in patients with previous left ventricular ballooning syndrome. Eur Heart J
0: ehp325v1-ehp325
[Abstract][Full Text]
Kent, L. K., Weston, C. A., Heyer, E. J., Sherman, W., Prudic, J.
(2009). Successful Retrial of ECT Two Months After ECT-Induced Takotsubo Cardiomyopathy. Am. J. Psychiatry
166: 857-862
[Full Text]
Ripa, C., Olivieri, F., Antonicelli, R.
(2009). Tako-Tsubo-Like Syndrome With Atypical Clinical Presentation: Case Report and Literature Review. ANGIOLOGY
60: 513-517
[Abstract]
Eitel, I., Schuler, G., Thiele, H.
(2009). Myocarditis mimicking Takotsubo cardiomyopathy or Takotsubo cardiomyopathy with secondary inflammation?. Eur J Heart Fail
11: 809-809
[Full Text]
Omerovic, E.
(2009). Did Jesus die of a 'broken heart'?. Eur J Heart Fail
11: 729-731
[Full Text]
Heggemann, F., Weiss, C., Hamm, K., Kaden, J., Suselbeck, T., Papavassiliu, T., Borggrefe, M., Haghi, D.
(2009). Global and regional myocardial function quantification by two-dimensional strain in Takotsubo cardiomyopathy. Eur J Echocardiogr
10: 760-764
[Abstract][Full Text]
Rolf, A., Nef, H. M., Mollmann, H., Troidl, C., Voss, S., Conradi, G., Rixe, J., Steiger, H., Beiring, K., Hamm, C. W., Dill, T.
(2009). Immunohistological basis of the late gadolinium enhancement phenomenon in tako-tsubo cardiomyopathy. Eur Heart J
30: 1635-1642
[Abstract][Full Text]
Latib, A., Ielasi, A., Montorfano, M., Colombo, A.
(2009). Broken heart syndrome: tako-tsubo cardiomyopathy. CMAJ
180: 1033-1034
[Full Text]
Ghosh, A. K, Hatfield, E., Connolly, S.
(2009). Catecholamine-induced transient myocardial dysfunction. BMJ Case Reports
2009: bcr1220081349-bcr1220081349
[Abstract][Full Text]
Lee, S. J., Kang, J. G., Ryu, O. H., Kim, C. S., Ihm, S.-H., Choi, M. G., Yoo, H. J., Hong, K. S.
(2009). The relationship of thyroid hormone status with myocardial function in stress cardiomyopathy. Eur J Endocrinol
160: 799-806
[Abstract][Full Text]
Abraham, J., Mudd, J. O., Kapur, N., Klein, K., Champion, H. C., Wittstein, I. S.
(2009). Stress Cardiomyopathy After Intravenous Administration of Catecholamines and Beta-Receptor Agonists. J Am Coll Cardiol
53: 1320-1325
[Abstract][Full Text]
Yousuf, M. A., Adjei, S., Kinder, B.
(2009). A 58-Year-Old Woman With ST-Segment Elevation, Seizures, and Altered Mental Status in the Setting of Opiate Withdrawal. Chest
135: 1098-1101
[Full Text]
Chen, F., Kan, H., Hobbs, G., Finkel, M. S.
(2009). p38 MAP kinase inhibitor reverses stress-induced myocardial dysfunction in vivo. J. Appl. Physiol.
106: 1132-1141
[Abstract][Full Text]
KUBZANSKY, L. D., KOENEN, K. C.
(2009). Is posttraumatic stress disorder related to development of heart disease? An update*. Cleveland Clinic Journal of Medicine
76: S60-S65
[Abstract][Full Text]
Coons, J. C., Barnes, M., Kusick, K.
(2009). Takotsubo cardiomyopathy. Am J Health Syst Pharm
66: 562-566
[Abstract][Full Text]
Meimoun, P., Malaquin, D., Benali, T., Boulanger, J., Zemir, H., Tribouilloy, C.
(2009). Transient impairment of coronary flow reserve in tako-tsubo cardiomyopathy is related to left ventricular systolic parameters. Eur J Echocardiogr
10: 265-270
[Abstract][Full Text]
Bijulal, S., Harikrishnan, S., Namboodiri, N., Ajitkumar, V. K, Gupta, D., Mathuranath, P S
(2009). Tako-tsubo cardiomyopathy in a patient with myasthenia gravis crisis: a rare clinical association. BMJ Case Reports
2009: bcr0620080182-bcr0620080182
[Abstract][Full Text]
Derrick, D.
(2009). The"Broken Heart Syndrome": Understanding Takotsubo Cardiomyopathy. Crit Care Nurse
29: 49-57
[Full Text]
POZUELO, L., TESAR, G., ZHANG, J., PENN, M., FRANCO, K., JIANG, W.
(2009). Depression and heart disease: What do we know, and where are we headed?. Cleveland Clinic Journal of Medicine
76: 59-70
[Abstract][Full Text]
Guerrero, J., Majid, A., Ernst, A.
(2009). Cardiogenic Shock Secondary to Tako-tsubo Syndrome After Debridement of Malignant Endobronchial Obstruction. Chest
135: 217-220
[Abstract][Full Text]
Burg, M. M., Graeber, B., Vashist, A., Collins, D., Earley, C., Liu, J., Lampert, R., Soufer, R.
(2009). Noninvasive Detection of Risk for Emotion Provoked Myocardial Ischemia. Psychosom. Med.
71: 14-20
[Abstract][Full Text]
Angelini, P.
(2009). Midventricular Variant of Transient Apical Ballooning: A Likely Demonstration of Its Pathophysiologic Mechanism. Mayo Clin Proc.
84: 92-93
[Full Text]
Akashi, Y. J., Goldstein, D. S., Barbaro, G., Ueyama, T.
(2008). Takotsubo Cardiomyopathy: A New Form of Acute, Reversible Heart Failure. Circulation
118: 2754-2762
[Full Text]
Eitel, I., Behrendt, F., Schindler, K., Kivelitz, D., Gutberlet, M., Schuler, G., Thiele, H.
(2008). Differential diagnosis of suspected apical ballooning syndrome using contrast-enhanced magnetic resonance imaging. Eur Heart J
29: 2651-2659
[Abstract][Full Text]
Afonso, L., Bachour, K., Awad, K., Sandidge, G.
(2008). Takotsubo cardiomyopathy: pathogenetic insights and myocardial perfusion kinetics using myocardial contrast echocardiography. Eur J Echocardiogr
9: 849-854
[Abstract][Full Text]
Bandettini, W P, Arai, A E
(2008). Advances in clinical applications of cardiovascular magnetic resonance imaging. Heart
94: 1485-1495
[Abstract][Full Text]
Whitten, S. E.
(2008). Systolic Heart Failure in a Patient With Hypertrophic Obstructive Cardiomyopathy: A Potentially Life-Threatening Complication. Crit Care Nurse
28: 44-52
[Full Text]
Roy-Byrne, P. P., Davidson, K. W., Kessler, R. C., Asmundson, G. J.G., Goodwin, R. D., Kubzansky, L., Lydiard, R. B., Massie, M. J., Katon, W., Laden, S. K., Stein, M. B.
(2008). Anxiety Disorders and Comorbid Medical Illness. Focus
6: 467-485
[Abstract][Full Text]
Parulekar, P, Khawaja, M Z O, McWilliams, E T
(2008). Chest pain after emotional and physical upset. BMJ
337: a107-a107
[Full Text]
De Santis, V., Vitale, D., Tritapepe, L., Greco, C., Pietropaoli, P.
(2008). Use of Levosimendan for Cardiogenic Shock in a Patient with the Apical Ballooning Syndrome. ANN INTERN MED
149: 365-367
[Full Text]
Zywica, K., Jenni, R., Pellikka, P.A., Faeh-Gunz, A., Seifert, B., Attenhofer Jost, C.H.
(2008). Dynamic left ventricular outflow tract obstruction evoked by exercise echocardiography: prevalence and predictive factors in a prospective study. Eur J Echocardiogr
9: 665-671
[Abstract][Full Text]
Baumert, M., Lambert, G. W., Dawood, T., Lambert, E. A., Esler, M. D., McGrane, M., Barton, D., Nalivaiko, E.
(2008). QT interval variability and cardiac norepinephrine spillover in patients with depression and panic disorder. Am. J. Physiol. Heart Circ. Physiol.
295: H962-H968
[Abstract][Full Text]
Bergman, B. R., Reynolds, H. R., Skolnick, A. H., Castillo, D.
(2008). A Case of Apical Ballooning Cardiomyopathy Associated with Duloxetine. ANN INTERN MED
149: 218-219
[Full Text]
Schummer, C., Wirsing, M., Schummer, W.
(2008). The Pivotal Role of Vasopressin in Refractory Anaphylactic Shock. Anesth. Analg.
107: 620-624
[Abstract][Full Text]
Bybee, K. A., Prasad, A.
(2008). Stress-Related Cardiomyopathy Syndromes. Circulation
118: 397-409
[Full Text]
Crimi, E., Baggish, A., Leffert, L., Pian-Smith, M. C.M., Januzzi, J. L., Jiang, Y.
(2008). Acute Reversible Stress-Induced Cardiomyopathy Associated with Cesarean Delivery under Spinal Anesthesia. Circulation
117: 3052-3053
[Full Text]
Schwenk, T. L., Spitters, C. E., Lippi, G., Targher, G., Farzaneh-Far, R., Farzaneh-Far, A., Wilbert-Lampen, U., Steinbeck, G.
(2008). Cardiovascular events during World Cup soccer.. NEJM
358: 2408-2408
[Full Text]
Ketterer, M. W., Knysz, W., Keteyian, S.J., Schairer, J., Jafri, S., Alam, M., Farha, A.J., Deveshwar, S.
(2008). Cardiovascular Symptoms in Coronary-Artery Disease Patients Are Strongly Correlated With Emotional Distress. Psychosomatics
49: 230-234
[Abstract][Full Text]
Ionescu, A.
(2008). Subaortic dynamic obstruction: a contributing factor to haemodynamic instability in tako-tsubo syndrome?. Eur J Echocardiogr
9: 384-385
[Abstract][Full Text]
Kogan, A., Ghosh, P., Schwammenthal, E., Raanani, E.
(2008). Takotsubo Syndrome After Cardiac Surgery. Ann. Thorac. Surg.
85: 1439-1441
[Abstract][Full Text]
Dimsdale, J. E.
(2008). Psychological Stress and Cardiovascular Disease. J Am Coll Cardiol
51: 1237-1246
[Abstract][Full Text]
Ramaraj, R.
(2008). A pathophysiological study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography. Eur Heart J
29: 681-681
[Full Text]
Yoshida, T., Hibino, T., Kako, N., Murai, S., Oguri, M., Kato, K., Yajima, K., Ohte, N., Yokoi, K., Kimura, G.
(2008). A pathophysiological study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography: reply. Eur Heart J
29: 681-682
[Full Text]
Nanda, S., Bhatt, S. P., Dale, T. H., Kurowski, V., Burgdorf, C., Radke, P. W.
(2008). Tako-tsubo Cardiomyopathy: An Insight Into Pathogenesis. Chest
133: 583-584
[Full Text]
Holman, E. A., Silver, R. C., Poulin, M., Andersen, J., Gil-Rivas, V., McIntosh, D. N.
(2008). Terrorism, Acute Stress, and Cardiovascular Health: A 3-Year National Study Following the September 11th Attacks. Arch Gen Psychiatry
65: 73-80
[Abstract][Full Text]
Fazal, I. A, Alfakih, K., Walsh, J. T
(2007). Takotsubo Cardiomyopathy. JRSM
100: 573-575
[Full Text]
Meimoun, P., Malaquin, D., Benali, T.
(2007). Reply to the letter to the editor by F. Tona et al.. Eur J Echocardiogr
8: 413-415
[Full Text]
Hakeem, A., Marks, A. D., Bhatti, S., Chang, S. M.
(2007). When the Worst Headache Becomes the Worst Heartache!. Stroke
38: 3292-3295
[Abstract][Full Text]
Yoshida, T., Hibino, T., Kako, N., Murai, S., Oguri, M., Kato, K., Yajima, K., Ohte, N., Yokoi, K., Kimura, G.
(2007). A pathophysiologic study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography. Eur Heart J
28: 2598-2604
[Abstract][Full Text]
Nef, H. M., Mollmann, H., Kostin, S., Troidl, C., Voss, S., Weber, M., Dill, T., Rolf, A., Brandt, R., Hamm, C. W., Elsasser, A.
(2007). Tako-Tsubo cardiomyopathy: intraindividual structural analysis in the acute phase and after functional recovery. Eur Heart J
28: 2456-2464
[Abstract][Full Text]
Guerrero, J., Majid, A., Feller-Kopman, D., Morgan, R., Anantham, D., Ernst, A.
(2007). CARDIOGENIC SHOCK SECONDARY TO TAKOTSUBO SYNDROME AFTER DEBRIDEMENT OF MALIGNANT ENDOBRONCHIAL OBSTRUCTION. Chest Meeting
132: 674a-674
[Abstract]
Nef, H. M, Mollmann, H., Elsasser, A.
(2007). Tako-tsubo cardiomyopathy (apical ballooning). Heart
93: 1309-1315
[Full Text]
Frey, N., Katus, H. A., Giannitsis, E.
(2007). The Tako-Tsubo Syndrome: An Underappreciated, Novel Disease Entity. Chest
132: 743-744
[Full Text]
Kurowski, V., Kaiser, A., von Hof, K., Killermann, D. P., Mayer, B., Hartmann, F., Schunkert, H., Radke, P. W.
(2007). Apical and Midventricular Transient Left Ventricular Dysfunction Syndrome (Tako-Tsubo Cardiomyopathy)* Frequency, Mechanisms, and Prognosis. Chest
132: 809-816
[Abstract][Full Text]
Ramaraj, R.
(2007). Stress cardiomyopathy: aetiology and management. Postgrad. Med. J.
83: 543-546
[Abstract][Full Text]
Elesber, A. A., Prasad, A., Lennon, R. J., Wright, R. S., Lerman, A., Rihal, C. S.
(2007). Four-Year Recurrence Rate and Prognosis of the Apical Ballooning Syndrome. J Am Coll Cardiol
50: 448-452
[Abstract][Full Text]
Ziegelstein, R. C.
(2007). Acute Emotional Stress and Cardiac Arrhythmias. JAMA
298: 324-329
[Abstract][Full Text]
Samuels, M. A.
(2007). The Brain-Heart Connection. Circulation
116: 77-84
[Full Text]
Vanacker, A., Meersseman, W., Knockaert, D. C., Wilmer, A., Blockmans, D.
(2007). A 42-Year-Old Woman With Sudden Onset of Back Pain and Severe Dyspnea. Chest
131: 1595-1598
[Full Text]
Buchholz, S., Rudan, G.
(2007). Tako-tsubo syndrome on the rise: a review of the current literature. Postgrad. Med. J.
83: 261-264
[Abstract][Full Text]
Kurisu, S., Inoue, I., Kawagoe, T., Ishihara, M., Shimatani, Y., Nakama, Y., Kagawa, E.
(2007). Pressure tracings in obstructive Tako-Tsubo cardiomyopathy. Eur J Heart Fail
9: 317-319
[Abstract][Full Text]
Prasad, A.
(2007). Apical Ballooning Syndrome: An Important Differential Diagnosis of Acute Myocardial Infarction. Circulation
115: e56-e59
[Full Text]
Vultaggio, A., Matucci, A., Del Pace, S., Simonetti, I., Parronchi, P., Rossi, O., Maggi, E., Gensini, G., Romagnani, S.
(2007). Tako-Tsubo-like syndrome during anaphylactic reaction. Eur J Heart Fail
9: 209-211
[Abstract][Full Text]
Wu, G. Y., Doshi, A. A., Haas, G. J.
(2007). Pheochromocytoma induced cardiogenic shock with rapid recovery of ventricular function. Eur J Heart Fail
9: 212-214
[Abstract][Full Text]
Olshansky, B.
(2007). Placebo and Nocebo in Cardiovascular Health: Implications for Healthcare, Research, and the Doctor-Patient Relationship. J Am Coll Cardiol
49: 415-421
[Abstract][Full Text]
Heaton, K. W
(2006). Faints, fits, and fatalities from emotion in Shakespeare's characters: survey of the canon. BMJ
333: 1335-1338
[Abstract][Full Text]
Gianni, M., Dentali, F., Lonn, E.
(2006). Apical ballooning syndrome, emotional stress and women: reply. Eur Heart J
27: 2908-2908
[Full Text]
Culic, V.
(2006). Apical ballooning syndrome, emotional stress and women. Eur Heart J
27: 2907-2908
[Full Text]
Iqbal, M B., Moon, J. C, Guttmann, O. P, Shanahan, P., Goadsby, P. J, Holdright, D. R
(2006). Stress, emotion and the heart: tako-tsubo cardiomyopathy. Postgrad. Med. J.
82: e29-e29
[Abstract][Full Text]
Van de Walle, S. O. A., Gevaert, S. A., Gheeraert, P. J., De Pauw, M., Gillebert, T. C.
(2006). Transient Stress-Induced Cardiomyopathy With an 'Inverted Takotsubo' Contractile Pattern. Mayo Clin Proc.
81: 1499-1502
[Abstract][Full Text]
Tofler, G. H., Muller, J. E.
(2006). Triggering of Acute Cardiovascular Disease and Potential Preventive Strategies. Circulation
114: 1863-1872
[Full Text]
Haghi, D., Athanasiadis, A., Papavassiliu, T., Suselbeck, T., Fluechter, S., Mahrholdt, H., Borggrefe, M., Sechtem, U.
(2006). Right ventricular involvement in Takotsubo cardiomyopathy. Eur Heart J
27: 2433-2439
[Abstract][Full Text]