5
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Takotsubo cardiomyopathy in patients with borderline stenosis of the left anterior descending artery and vasospastic angina: to stent or not to stent? A case report

      case-report

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Takotsubo cardiomyopathy (TCM) is a complex disease that resembles the clinical presentation of acute myocardial infarction with non-obstructive coronary arteries. The aetiology remains elusive despite the comprehensive nature of current guidelines meticulously detailing the diagnostic process.

          Case summary

          We present the case of a 64-year-old female who presented with a clinical profile consistent with non-ST elevation myocardial infarction, confirmed by elevated cardiac enzyme levels. Echocardiography raised suspicions of TCM. Angiography presented a challenge, revealing a 65% stenosis of the left anterior descending artery (LAD). Based on the collected evidence, we decided to delay and ultimately forgo LAD revascularization while identifying epicardial vasospasm through a provocation test as a possible cause underlying TCM.

          Discussion

          Conducting an acetylcholine provocation test, as recommended by the European Society of Cardiology guidelines for patients with ischaemia and no obstructive coronary artery disease unveiled severe diffuse vasospasm affecting both the LAD and circumflex arteries. The intricate interplay of pathophysiological mechanisms and clinical presentations necessitates ongoing exploration to uncover the mysteries and refine our diagnostic and therapeutic strategies.

          Related collections

          Most cited references15

          • Record: found
          • Abstract: found
          • Article: not found

          Neurohumoral features of myocardial stunning due to sudden emotional stress.

          Reversible left ventricular dysfunction precipitated by emotional stress has been reported, but the mechanism remains unknown. We evaluated 19 patients who presented with left ventricular dysfunction after sudden emotional stress. All patients underwent coronary angiography and serial echocardiography; five underwent endomyocardial biopsy. Plasma catecholamine levels in 13 patients with stress-related myocardial dysfunction were compared with those in 7 patients with Killip class III myocardial infarction. The median age of patients with stress-induced cardiomyopathy was 63 years, and 95 percent were women. Clinical presentations included chest pain, pulmonary edema, and cardiogenic shock. Diffuse T-wave inversion and a prolonged QT interval occurred in most patients. Seventeen patients had mildly elevated serum troponin I levels, but only 1 of 19 had angiographic evidence of clinically significant coronary disease. Severe left ventricular dysfunction was present on admission (median ejection fraction, 0.20; interquartile range, 0.15 to 0.30) and rapidly resolved in all patients (ejection fraction at two to four weeks, 0.60; interquartile range, 0.55 to 0.65; P<0.001). Endomyocardial biopsy showed mononuclear infiltrates and contraction-band necrosis. Plasma catecholamine levels at presentation were markedly higher among patients with stress-induced cardiomyopathy than among those with Killip class III myocardial infarction (median epinephrine level, 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 [interquartile range, 1709 to 2910] vs. 1100 pg per milliliter [interquartile range, 914 to 1320]; and dopamine level, 111 pg per milliliter [interquartile range, 106 to 146] vs. 61 pg per milliliter [interquartile range, 46 to 77]; P<0.005 for all comparisons). Emotional stress can precipitate severe, reversible left ventricular dysfunction in patients without coronary disease. Exaggerated sympathetic stimulation is probably central to the cause of this syndrome. Copyright 2005 Massachusetts Medical Society.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            International Expert Consensus Document on Takotsubo Syndrome (Part II): Diagnostic Workup, Outcome, and Management

            Abstract The clinical expert consensus statement on takotsubo syndrome (TTS) part II focuses on the diagnostic workup, outcome, and management. The recommendations are based on interpretation of the limited clinical trial data currently available and experience of international TTS experts. It summarizes the diagnostic approach, which may facilitate correct and timely diagnosis. Furthermore, the document covers areas where controversies still exist in risk stratification and management of TTS. Based on available data the document provides recommendations on optimal care of such patients for practising physicians.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Pathophysiology of Takotsubo Syndrome

              Originally described by Japanese authors in the 1990s, Takotsubo syndrome (TTS) generally presents as an acute myocardial infarction characterized by severe left ventricular dysfunction. TTS, however, differs from an acute coronary syndrome because patients have generally a normal coronary angiogram and left ventricular dysfunction, which extends beyond the territory subtended by a single coronary artery and recovers within days or weeks. The prognosis was initially thought to be benign, but subsequent studies have demonstrated that both short-term mortality and long-term mortality are higher than previously recognized. Indeed, mortality reported during the acute phase in hospitalized patients is ≈4% to 5%, a figure comparable to that of ST-segment-elevation myocardial infarction in the era of primary percutaneous coronary interventions. Despite extensive research, the cause and pathogenesis of TTS remain incompletely understood. The aim of the present review is to discuss the pathophysiology of TTS with particular emphasis on the role of the central and autonomic nervous systems. Different emotional or psychological stressors have been identified to precede the onset of TTS. The anatomic structures that mediate the stress response are found in both the central and autonomic nervous systems. Acute stressors induce brain activation, increasing bioavailability of cortisol and catecholamine. Both circulating epinephrine and norepinephrine released from adrenal medullary chromaffin cells and norepinephrine released locally from sympathetic nerve terminals are significantly increased in the acute phase of TTS. This catecholamine surge leads, through multiple mechanisms, that is, direct catecholamine toxicity, adrenoceptor-mediated damage, epicardial and microvascular coronary vasoconstriction and/or spasm, and increased cardiac workload, to myocardial damage, which has a functional counterpart of transient apical left ventricular ballooning. The relative preponderance among postmenopausal women suggests that estrogen deprivation may play a facilitating role, probably mediated by endothelial dysfunction. Despite the substantial improvement in our understanding of the pathophysiology of TTS, a number of knowledge gaps remain.
                Bookmark

                Author and article information

                Contributors
                Role: Handling Editor
                Role: Editor
                Role: Editor
                Role: Editor
                Role: Editor
                Journal
                Eur Heart J Case Rep
                Eur Heart J Case Rep
                ehjcr
                European Heart Journal. Case Reports
                Oxford University Press (UK )
                2514-2119
                September 2024
                13 September 2024
                13 September 2024
                : 8
                : 9
                : ytae452
                Affiliations
                Department of Interventional Cardiology, Institute of Cardiology, Jagiellonian University Medical College , św. Anny 12, 31-007 Kraków, Poland
                Doctoral School of Medical and Health Sciences, 162261 Jagiellonian University , Krakow, Poland
                Department of Interventional Cardiology, Institute of Cardiology, Jagiellonian University Medical College , św. Anny 12, 31-007 Kraków, Poland
                Department of Interventional Cardiology, The John Paul II Hospital , Prądnicka 80, 31-202 Kraków, Poland
                Department of Interventional Cardiology, Institute of Cardiology, Jagiellonian University Medical College , św. Anny 12, 31-007 Kraków, Poland
                Department of Interventional Cardiology, The John Paul II Hospital , Prądnicka 80, 31-202 Kraków, Poland
                Department of Interventional Cardiology, Institute of Cardiology, Jagiellonian University Medical College , św. Anny 12, 31-007 Kraków, Poland
                Department of Interventional Cardiology, The John Paul II Hospital , Prądnicka 80, 31-202 Kraków, Poland
                Department of Interventional Cardiology, Institute of Cardiology, Jagiellonian University Medical College , św. Anny 12, 31-007 Kraków, Poland
                Department of Interventional Cardiology, The John Paul II Hospital , Prądnicka 80, 31-202 Kraków, Poland
                Department of Cardiology 5th Military Policlinical Hospital , Wrocławska 1-3; Kraków, Poland
                Author notes
                Corresponding author. Tel: +48501603091, Email: b.guzik@ 123456uj.edu.pl .

                Conflict of interest: None declared for all the authors.

                Author information
                https://orcid.org/0000-0002-3333-6454
                https://orcid.org/0000-0003-2577-2923
                https://orcid.org/0000-0001-6883-8633
                https://orcid.org/0000-0002-2945-3674
                https://orcid.org/0000-0002-0630-8394
                Article
                ytae452
                10.1093/ehjcr/ytae452
                11425307
                39328845
                526e3b25-f973-413e-bf5b-3041a520fba6
                © The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License ( https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.

                History
                : 30 January 2024
                : 26 May 2024
                : 15 August 2024
                : 26 September 2024
                Page count
                Pages: 5
                Funding
                Funded by: Abbott Medical;
                Categories
                Case Report
                AcademicSubjects/MED00200
                Eurheartj/39
                Eurheartj/41
                Eurheartj/15
                Eurheartj/17

                cardiomyopathy,heart failure,myocardial infarction,takotsubo,oct,case report

                Comments

                Comment on this article