Article, Cardiology

All stressed out and no pump to go

All stressed out and no pump to go

A 57-year-old woman presented to the emergency department (ED) with chest pain and electrocardiographic (EKG) changes that were suggestive of an ST-segment elevation myocardial infarction . Her pain was not eased by aggressive treatment with aspirin, b-blockers, antithrombins, nitrates, HMG-coenzyme A reductase inhib- itors, and antithrombolytics.

The patient’s echocardiogram showed severely reduced left ventricular (LV) function with apical and lateral wall akinesis. At catheterization, normal coronaries and persistent LV dysfunction were found. Study findings on the presence of a Hypercoagulable state were negative. The patient developed mild pulmonary edema but had an uneventful course in the hospital. Four weeks after treatment, her left ventricle showed a normal ejection fraction (EF). In this article, we discuss the case patient and the entity of Takotsubo cardiomyopathy (CM).

That stress plays a role in certain diseases seems obvious. However, it is rare that a syndrome induced by stress can mimic another disorder to the extent that whole treatment algorithms that are not only not helpful but also detrimental may be followed.

Takotsubo CM is a newly described disorder of the heart in which a severe response to adrenergic stimulus occurs in a mostly female postmenopausal population.

A 57-year-old postmenopausal white female RN developed precordial chest discomfort and shortness of breath at work when her employers notified her that a patient had called in to complain about her. She became quite anxious and was convinced that her symptoms were caused by anxiety only. At the prodding of her (mostly physician) employers, she went to the ED, where she was immediately brought to the back area and underwent an EKG. Her initial pain was a 5 on scale of 1 to 10. She did have some back pain as well. She noted no prior cardiac history, but she was being treated for hyperten- sion and hyperlipidemia. Her medications were spironolactone, omeprazole, rosuvastatin, and candesartan. Her family history was unremarkable, and she never smoked. She did undergo 2 angioplasties of the renal arteries for fibromuscular dysplasia. On physical examination, the patient was an anxious excitable woman noted to be in sinus tachycardia at 125/min, with 1 to 2 premature ventricular depolarizations per minute. A 21-mm Hg difference between the right and left sides was noted on her systolic blood pressure. Her lungs were clear. A soft S3 could be heard. Hepatosplenomegaly, abdominal tenderness, rash, edema or cyanosis, bleeding, and joint effu-

sions were not noted on the rest of her examination findings.

The patient’s initial EKG showed sinus rhythm at 106 with left-axis deviation and 0.5-mm ST-segment elevation in leads I and aVL (Fig. 1). Sublingual nitroglycerin decreased her pain, but it returned almost immediately. A second EKG then showed a full 1-mm ST-segment elevation in the high lateral leads. A right-sided and

posterior EKG was conducted, which showed normal ST-T waves. Echocardiography was performed at the bedside while informed consent for thrombolytics was asked of her. The echocardiogram showed LV hypertrophy with severely reduced EF of approximately 20%. There was akinesis of the apex and lateral and apicoinferior walls with preserved or even hyperdynamic basal wall/outflow tract function (Fig. 2). Trivial Mitral regurgitation (MR) was noted. There was no right ventricular dysfunction or elevated pulmonary artery pressure to suggest a pulmonary embolism; no sign of a dissection, ventricular septal defect, or papillary rupture was evident (Fig. 1).

The patient received 2 doses of 10-mg reteplase and received intravenous and subcutaneous low-molecular weight heparin, full intravenous b blockade with IV metoprolol 5 mg times three, simvastatin 40 mg PO, and acetylsalicylic acid 160 mg PO. Intravenous nitroglycerin was started. The patient failed to achieve reduction in pain and in ST-segment elevation; she was flown to a nearby cardiac catheterization laboratory in anticipation of thera- peutic intervention.

Cardiac catheterization revealed the presence of normal coronaries in a right dominant system and severely reduced LV dysfunction similar to the ED echocardiographic findings [1] (Figs. 3A, B, and 4). A mild to moderately elevated pulmonary capillary wedge pressure of 28 mm Hg presaged the onset of pulmonary edema. The patient had an otherwise uneventful hospital course and was discharged on day 4. Her peak creatinine phosphokinase (CPK) level was 286 IU, with a relative index of 15.3%. The troponin level however rose to a high of 113 ng/mL. The findings from a hypercoagulation panel were negative. The patient was discharged with prescriptions for acetylsalicylic acid, clopidogrel, ramipril, and carvedilol (Fig. 2).

Six weeks after her hospitalization, the patient had a repeat echocardiogram that showed normalization of LV function with an estimated EF of 65%. She had neither wall motion abnormalities nor MR. She was able to return to full-time work with b-blockers, an angiotensin receptor blocker, clopidogrel, aldactone, and aspirin. She reported no physical limitation in her daily life and has had no recurrence of chest pain. She now works in the back-office and does not take frontline phone calls on Mondays.

This distinct syndrome characterized by anteroapical LV stunning and dynamic LV outflow obstruction was de- scribed in as early as 2000. The term Takotsubo (Japanese for octopus pot or trap) was first given to the entity after several Japanese case series described the unique chest pain syndrome [2-4]. Characteristic ballooning of the apex and lateral and inferoapical walls with normal coronaries and resolution of the LV dysfunction characterize the disorder [5-9]. A striking preponderance of female patients, often Postmenopausal women, as compared with male patients (6:1) was subsequently identified [1,2]. Other terms that have been given to the distinct presentation include LV apical ballooning syndrome, broken heart syndrome, and

Fig. 1 Twelve-lead EKG showing sinus rhythm with minimal ST-segment elevation in leads I and aVL.

ampulla CM [2,10-12]. That a stressful life event preceded the disorder in a high percentage of patients was noted shortly after the event began to be described. Precursor events have been listed and include news of the death of a loved one, quarreling, severe pain, public performance, financial losses, an earthquake, excess Alcohol intake, nosebleeds, gastrointestinal bleeding, intensive care unit admission/syndrome, intracranial hemorrhage, spousal de- parture/marital discord, respiratory failure, pneumothorax, hypoglycemia, traffic accidents, polyangiitis, postoperative and postanesthetic states, diabetic ketoacidosis, hypoten- sion, methicillin-resistant staphylococcal meningitis, exac- erbations of chronic disease such as myasthenia gravis, and cocaine use [1,2,5,6,10-25]. Some series listed as a requirement no history of MI, subarachnoid hemorrhage, pheochromocytoma, and drug excess (eg, cocaine), whereas other series and case reports listed these as causes of the syndrome [9,26].

Initially, it was thought that spasm and/or thrombus could lead to the singularly characteristic LV dysfunction. Abnormal Thrombolysis In Myocardial Infarction frame counts in all major coronary vessels (these show whether there is delay in clearing of contrast after the injection of a coronary suggesting decreased perfusion), abnormal perfu-

sion study findings, and exceptionally elevated levels of circulating epinephrine and norepinephrine have caused the culprit to be suspected of being adrenergic overdrive

Fig. 2 Emergency department-taken echocardiogram in the parasternal long-axis view showing hyperdynamic basal segments and characteristic ballooning of the septum and apex with akinetic LV apex and lateral and posterior walls. The estimated EF on the echocardiogram was 20%.

or catecholamine-induced microvascular dysfunction [5,12,27]. The reason for the differential response of the basal segments of the heart vs the apical segments and the characteristic apical ballooning is not known. In a rat model of emotional stress, typical apical LV ballooning that could be prevented by preadministration of adrenergic

Fig. 3 A, coronary angiogram of the left main coronary injection showing the normal left anterior descending artery, ramus branch, and obtuse marginal arteries. B, Coronary angiogram of the right coronary injection showing a widely patent artery.

Fig. 4 Left ventriculogram showing akinetic apex and character- istic oyster pot-like appearance with hyperkinetic basal segments.

b– and a-blockers could be induced [5]. After the initial spate of articles, reports and series on mostly white patients began to surface in the United States [11,22]. Unsolved yet are the very characteristic distribution of the LV ballooning dysfunction and the syndrome’s predilection for women.

The clinical presentation of this stress CM mimics that of typical STEMI or non-STEMI (NSTEMI). Patients present with the typical tachyarrhythmia and bradyar- rhythmia seen in acute MI (AMI) but may also progress to pulmonary edema and cardiogenic shock. Apical LV dysfunction may lead to elevated LV end-diastolic pressure (LVEDP); in addition, MR is common (possibly as a result of dilation plus reconfiguring the anatomy of the mitral ring). Dynamic LV outflow obstruction is fairly characteristic because of the retained and even hyper- dynamic contraction of the LV basal wall segments; this latter phenomenon can further contribute to elevated LVEDP, making congestive heart failure more common than other acute coronary syndromes (ACSs). Left ventricular rupture, ventricular septal defect formation, and rupture of the papillary muscle have both been reported [27-29]. In several series, cardiogenic shock is reported with a higher frequency, with 6 of 13 patients in one study requiring intraaortic balloon counterpulsation [11,24,27,30,31].

Electrocardiographic presentations can be quite variable: ST-segment elevations similar to those in STEMI are common but not the rule. Often, deep T-wave inversions follow where the ST-segment elevations occurred in the acute setting rather

than the classic pattern of Q-wave development [32]. When pathologic Q waves develop, they often disappear. The most common leads to show ST-segment elevation are leads V1 through V3 and, occasionally, leads I and aVL.

One study noted that reciprocal changes in the inferior leads were particularly uncommon in patients with Takotsubo CM as compared with patients with a true anterior MI. In that study, lateral leads V4 through V6 had an ST-segment elevation more commonly than did anterior precordial leads V1 through V3; furthermore, ventricular tachycardia and ventricular fibrillation have been reported to occur in 8% to 12% of patients, rates possibly higher than those in other subsets of patients with AMI. Torsade de pointes is not uncommon [33]. This would seem to be related to the high catecholamine state involved. A very prolonged QTc is fairly characteristic, as is the disappearance of the pronged QT after 2 to 3 days. Late arrhythmias and heart block seem to be rare [31]. Invariably, these changes disappear over a variable period, usually within weeks.

Echocardiography and LV angiography show moderately to severely reduced EF with apical, anterolateral, and inferoapical akinesis with preservation of the basal wall function. Systolic anterior motion of the mitral valve is common, and an outflow gradient is detectable in a significant percentage of patients [12,29,34]. In single- photon emission computed tomography, 99mTc-tetrofosmin uptake is reduced but exists in the akinetic segments; it is felt that this residual perfusion is what preserves the myocardi- um, leading to eventual return to normal EF levels. It is theorized that this is a form of Myocardial stunning. Left ventriculography shows a characteristic ballooning of the apex and inferior/lateral walls not corresponding well to the distribution of any one major coronary artery [35]. Normal coronaries are found in most cases [2,9-11].

Laboratory abnormalities may not mimic those in STEMI or NSTEMI, although elevations of troponin and CPK levels have been reported. The peak CPK level is not usually found to correspond to the initial LV dysfunction seen. Widely varying troponin levels do not correlate with long-term outcomes or severity of LV dysfunction seen on echocardiography or angiography. Brain natriuretic peptide levels may rise precipitously but do not correlate with the long-term prognosis as they do in other ACSs. Plasma catecholamine levels in Takotsubo CM are markedly higher than in ACS and Killip class III heart failure from MI [23]. Takotsubo syndrome or CM has been relatively recently discovered or defined, and its unusual features raise several questions in terms of diagnosis and initial as well as follow- up treatments. There is practically no report of this condition in the emergency medicine literature, given that the ED is where most affected patients must often be presenting. Such patients may also be those we encounter in critical care settings with acute decompensation. How often do we see a patient under duress with Takotsubo CM and call it stress and then prescribe rest, anxiolytics, or perhaps b-blockers for

suspected mitral valve prolapse?

Current American Heart Association/American College of Cardiology guidelines suggest a 30-minute time frame during which to evaluate and prepare a STEMI patient for thrombolytic therapy when interventional catheterization laboratories are not available. A 90-minute Door-to-balloon time is considered as the gold standard for cases in which therapeutic stenting is planned; although not all patients with Takotsubo syndrome have STEMI, our patient met the criteria of having an ST-segment elevation and continued chest pain for immediate lysis and/ or intervention. Currently in the United States, we are still far from being able to offer immediate stenting to all patients with STEMI. Our patient’s failure to achieve symptom (pain) resolution in this setting prompted transfer when, in fact, no further intervention was actually needed. This raises several difficult questions that could make treatment of a patient with AMI more difficult. Should all chest pain patients undergo an echocardiography before being chosen to receive or to not receive thrombo- lytics? How can we avoid giving lytics when immediate interventional catheterization is not available? Should all patients be transferred/catheterized with ongoing chest pain? Should postmenopausal women with this classic clustering of features be assumed to have the condition and sent to the catheterization laboratory with no consideration for lytics? Finally, what actually are the optimal early and late treatments for this entity?

Most series suggested that recurrence is rare; however, there is limited to no long-term information, with the first report on this being only 5 years old. Follow-up treatment and risk factor management are not really discussed and are of interest because exposure to stress cannot be controlled for or avoided. Because the pathophysiology of Takotsubo CM seems to be related to adrenergic pulsing of the myocardium and small vessels, should b blockade be the cornerstone of early management and long-term management? If the answer to this is yes, should the patient have both a and b blockade to maximize resistance to the effects of norepinephrine and epinephrine? Would Calcium-channel blockers be useful if small vessel spasm plays a role? Are Antiplatelet agents as useful as they are in other ACSs? Do direct and indirect thrombin inhibitors have a salutary effect or are they not needed? Because the brain natriuretic peptide level does not predict or correlate with long-term LV dysfunction, should angiotensin-con- verting enzyme inhibitors and/or angiotensin receptor blockers be used based on the initial EF or not used based on the follow-up EF? Is there a role for HMG- coenzyme A reductase inhibitors in endothelial protection? Takotsubo CM is a unique syndrome with a mechanism unlike that of other ACSs, causing more questions to be raised regarding its classic management. It would seem almost intuitive that b-blockers could help mitigate the adrenergic response of the blood vessels and the LV outflow obstruction characteristic of Takotsubo CM. Theoretically, full b blockade could lead to a drop in LVEDP by reducing the afterload from the outflow obstruction. It would also

seem ideal for affected patients to maintain their b-blocker therapy on a long-term basis to mitigate the effects of adrenergic pulsing if another emotional stressor were to occur. If there is defective flow in the macrocirculation or microcirculation, is there a role for use of calcium-channel blockers in this entity? Awareness of this syndrome is important; rapid screening and identification, avoidance of lytics when possible, prompt and aggressive treatment of failure, and need for immediate use of b-blockers possibly even in higher doses than those in usual ACSs all characterize this entity.

The fact that affected patients present to the ED begs the need to investigate the Optimal treatment and makes us compelled to be aware of this completely reversible form of LV dysfunction and/or MI. Long-term data will hopefully become available, and insights into the best way to diagnose and implement treatment without delaying therapy for true STEMI and NSTEMI are awaited. As to how many cases have gone unrecognized is unknown. Whether patients can present with completely normal EKG findings or without the Troponin elevation that would trigger an admission is also not known, but the relatively minimal changes in our patient with a huge elevation in the troponin level and a relatively minimal increase in the CPK level demonstrate the lack of usual correlations with and prognostication of ST-segment changes, total CPK level, EF, or total troponin level.

Our institution has identified 4 more patients in the year since this case was identified: 1 patient was an intensive care unit patient whose symptoms developed during a stressful admission for diabetic ketoacidosis and the other

3 patients presented to the ED with what sounded like Atypical chest pain; 1 patient had EKG findings that were completely normal. Keen awareness and early recognition of this entity seem to be paramount for ED physicians, and the outcome of failure to admit or diagnose this potentially lethal entity should be avoided.

Marilyn Geninatti MD, FACEP Emergency Department Paradise Valley Hospital Phoenix, AZ 85032, USA

Marc Thames MD, FACC Department of Cardiology Paradise Valley Hospital Phoenix, AZ 85032, USA



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    Feeling bloated

    A 58-year-old man with well-controlled type 2 diabetes mellitus was found to have a well-differentiated adenocar- cinoma of the head of the pancreas during a workup of jaundice and weight loss. An attempted Whipple procedure was aborted because the mass invaded the superior mesenteric vascular axis, and only a palliative biliary bypass was performed. Two months later, recurrent cholestasis was alleviated by placement of a metallic biliary endoprosthesis followed by 6 weeks of neoadjuvant gemcitabine and external beam radiation therapy. Four months later, the patient reported a 1-week history of nausea, vomiting, and absence of bowel movement. His abdomen was distended, with preserved peristaltic sounds and increased sonority to percussion but no tenderness or guarding. A plain abdom- inal radiograph taken with the patient standing (Fig. 1) revealed a strikingly distended stomach (40 cm) and proximal duodenum, the previously placed common biliary duct stent (white arrowhead, panel A), the secondary pneumobilia (black arrows, panel A), and metallic clips (white arrows, panel A). A chest radiograph showed a marked elevation of the left hemidiaphragm.

    The patient presented with a combination of bgastric outlet obstructionQ and severe bgastroparesis.Q A nasogastric tube was placed, releasing 3 L of dark green gastrobiliary secretions. Endoscopic retrograde cholangiopancreatogra- phy showed a stricture in the proximal existent stent; therefore, a covered 10 x 40-mm wall stent (white arrow, panel B) was placed into the migrated stent (white arrowhead, panel B). An obstructing stricture in the

    descending duodenum below the biliary opening was alleviated by the successful placement of a duodenal self- expandable enteral metal stent (black arrow, panel B). A week after presentation, the patient was discharged home with restored oral intake.

    Acute massive gastric distension occurs particularly in patients with pathologic eating disorders or superior mesen- teric artery syndrome [1] and can cause lethal mucosal ischemia and necrosis [2,3], or mechanical hemodynamic catastrophe [4]. This case of chronic distension secondary to gastric outlet obstruction illustrates a particularly increased proximal gastric compliance [5]. The hyperglycemia [6] and hyperinsulinemia [7] secondary to type 2 diabetes mellitus

    Fig. 1 abdominal radiograph at presentation (A) reveals striking 40-cm Gastric dilatation and pneumobilia; and immediately after placement of a duodenal self-expanding enteral stent (B).

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