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A Transient Hypertrophic Cardiomyopathy?
Abstract
A Transient Hypertrophic Cardiomyopathy? Abstract. We report on a 79-year-old female patient after blunt chest trauma. Based on T-negative findings on 12-lead ECG and apical left ventricular hypertrophy on echocardiography and cardiac MRI examination, apical hypertrophic cardiopathy was postulated. Subsequently, it was shown that these findings were present only transiently and completely normalized in the course. The apical changes were not due to hypertrophy of cardiomyocytes but to myocardial edema. Both Takotsubo syndrome and contusio cordis were considered as causes.
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Yamaguchi syndrome or apical hypertrophic cardiomyopathy (HCM) is a unique variant of HCM. It is characterized by localized hypertrophy involving the left ventricular apex rather than the left ventricular septum. This syndrome has been traditionally seen in the Asian population, particularly those of Japanese descent. We present an interesting case of Yamaguchi syndrome seen in a Hispanic male.
A 48-year-old Hispanic male presented with epigastric tenderness and was admitted to the hospital for a non-ST-segment elevation myocardial infarction. His diagnostic catheterization revealed no significant coronary artery disease. However, his echocardiogram revealed apical hypertrophy and narrowing of the left ventricular cavity at the apex, consistent with Yamaguchi syndrome. Case reports such as ours serve to help clinicians broaden their differential diagnoses when approaching patients with acute coronary syndrome-like symptoms to include diagnoses such as Yamaguchi syndrome.
Apical variant hypertrophic cardiomyopathy (AHCM) is characterized by asymmetric hypertrophy of the left ventricular (LV) apex. T wave inversions of variable degree, particularly in the left precordial leads, and left ventricular hypertrophy (LVH) are common EKG findings in AHCM. Echocardiography is typically the initial imaging modality used in the diagnosis and evaluation of AHCM. The diagnosis is made when the LV apex has apical wall thickness of ≥ 15 mm or a ratio of apical to basal LV wall thickness of ≥ 1.3 at end-diastole. The use of microbubble contrast agents with echocardiography is helpful for visualization of the apex. Cardiac magnetic resonance (CMR) has the advantage of a large field of view and the ability to perform tissue characterization. Late gadolinium enhancement (LGE) sequences are essential in the assessment of potential areas of myocardial scarring. Cardiac computed tomography (CCT) has the advantage of being able to evaluate coronary arteries in addition to assessing cardiac anatomy and function. A “Solar Polar” map pattern is the characteristic feature of AHCM on myocardial perfusion imaging (MPI) in cases not associated with apical aneurysm (APA). Recognition of typical perfusion patterns in AHCM patients is not only important in the diagnostic evaluation of this disease process, but also for avoiding unnecessary and costly tests. The purpose of this article is to review the imaging features of AHCM from different imaging modalities and assess the value added of each modality in the diagnosis of AHCM.
The natural history, management, and outcome of takotsubo (stress) cardiomyopathy are incompletely understood.
The International Takotsubo Registry, a consortium of 26 centers in Europe and the United States, was established to investigate clinical features, prognostic predictors, and outcome of takotsubo cardiomyopathy. Patients were compared with age- and sex-matched patients who had an acute coronary syndrome.
Of 1750 patients with takotsubo cardiomyopathy, 89.8% were women (mean age, 66.8 years). Emotional triggers were not as common as physical triggers (27.7% vs. 36.0%), and 28.5% of patients had no evident trigger. Among patients with takotsubo cardiomyopathy, as compared with an acute coronary syndrome, rates of neurologic or psychiatric disorders were higher (55.8% vs. 25.7%) and the mean left ventricular ejection fraction was markedly lower (40.7±11.2% vs. 51.5±12.3%) (P<0.001 for both comparisons). Rates of severe in-hospital complications including shock and death were similar in the two groups (P=0.93). Physical triggers, acute neurologic or psychiatric diseases, high troponin levels, and a low ejection fraction on admission were independent predictors for in-hospital complications. During long-term follow-up, the rate of major adverse cardiac and cerebrovascular events was 9.9% per patient-year, and the rate of death was 5.6% per patient-year.
Patients with takotsubo cardiomyopathy had a higher prevalence of neurologic or psychiatric disorders than did those with an acute coronary syndrome. This condition represents an acute heart failure syndrome with substantial morbidity and mortality. (Funded by the Mach-Gaensslen Foundation and others; ClinicalTrials.gov number, NCT01947621.).
Stress cardiomyopathy (SC) is a transient form of acute heart failure triggered by stressful events and associated with a distinctive left ventricular (LV) contraction pattern. Various aspects of its clinical profile have been described in small single-center populations, but larger, multicenter data sets have been lacking so far. Furthermore, it remains difficult to quickly establish diagnosis on admission.
To comprehensively define the clinical spectrum and evolution of SC in a large population, including tissue characterization data from cardiovascular magnetic resonance (CMR) imaging; and to establish a set of CMR criteria suitable for diagnostic decision making in patients acutely presenting with suspected SC.
Prospective study conducted at 7 tertiary care centers in Europe and North America between January 2005 and October 2010 among 256 patients with SC assessed at the time of presentation as well as 1 to 6 months after the acute event.
Complete recovery of LV dysfunction.
Eighty-one percent of patients (n = 207) were postmenopausal women, 8% (n = 20) were younger women (aged ≤50 years), and 11% (n = 29) were men. A stressful trigger could be identified in 182 patients (71%). Cardiovascular magnetic resonance imaging data (available for 239 patients [93%]) revealed 4 distinct patterns of regional ventricular ballooning: apical (n = 197 [82%]), biventricular (n = 81 [34%]), midventricular (n = 40 [17%]), and basal (n = 2 [1%]). Left ventricular ejection fraction was reduced (48% [SD, 11%]; 95% confidence interval [CI], 47%-50%) in all patients. Stress cardiomyopathy was accurately identified by CMR using specific criteria: a typical pattern of LV dysfunction, myocardial edema, absence of significant necrosis/fibrosis, and markers for myocardial inflammation. Follow-up CMR imaging showed complete normalization of LV ejection fraction (66% [SD, 7%]; 95% CI, 64%-68%) and inflammatory markers in the absence of significant fibrosis in all patients.
The clinical profile of SC is considerably broader than reported previously. Cardiovascular magnetic resonance imaging at the time of initial clinical presentation may provide relevant functional and tissue information that might aid in the establishment of the diagnosis of SC.
Takotsubo cardiomyopathy (TTC) is an increasingly recognised acute cardiac syndrome, whose underlying pathophysiological mechanisms remain unknown. Inflammation might play a role as this has been shown in endomyocardial biopsies. The aim of this study was to assess inflammatory parameters in patients with TTC using a comprehensive cardiovascular magnetic resonance imaging (CMR) approach.
Thirty-seven patients with the suspected diagnosis of TTC underwent CMR. T2-weighted imaging to calculate the oedema ratio, T1-weighted imaging before and after contrast agent administration to calculate the global relative enhancement (gRE), and late gadolinium enhancement (LGE) imaging were performed.
In 11 patients CMR revealed the diagnosis of myocardial infarction (n = 7; 19%) or myocarditis (n = 4; 11%) with typical patterns of LGE. In all other patients (n = 26; 70%), no LGE was detected consistent with the diagnosis of TTC. Of these, in 16 patients (62%) both inflammatory markers (oedema ratio and gRE) were elevated with concomitant pericardial effusion, indicating acute inflammation. Follow-up CMR after 3 months showed complete normalisation of left ventricular function and inflammatory parameters in the absence of LGE and pericardial effusion.
This CMR study provides further insights into the pathophysiological mechanisms in TTC, supporting the contribution of an inflammatory process in the acute setting.
In this article, we report the autopsy findings of a 48-year-old man who sustained blunt trauma to the thorax. A medical record review revealed no history of cardiac disease. He presented to the hospital with a computed tomography-verified fracture of the left fourth and fifth ribs, and pulmonary and cardiac contusion. He was released from the hospital in stable condition at his own request 7 days later. Because of sudden deterioration, he was readmitted to the hospital the next day. Electrocardiogram detected cardiac arrhythmia on the 15th day after chest trauma. Electrocardiography detected pericardial effusion and severe mitral insufficiency resulting in left ventricular failure. Death was attributed to diffuse alveolar damage-complicating pneumonia due to cardiac contusion with mitral insufficiency occurring 25 days after hospital admission. Internal examination revealed diffuse fibrinous pericarditis, left atrial tear right above the anterior mitral valve leaflet with intrapericardial granulation tissue, and no sign of myocardial damage. Immunohistochemistry showed significantly more CD68-positive macrophages within tissue taken from the heart, a finding indicative of previous atrial and ventricular myocardial contusion. This case report demonstrates that routine hematoxylin and eosin staining may not always reveal significant myocardial damage.
Myocardial edema is one of the characteristic features in the pathogenesis of Takotsubo syndrome. We report a middle aged man who presented with typical clinical and echocardiographic features of apical variant of Takotsubo syndrome. However, a cardiovascular magnetic resonance study performed 10 days after presentation did not show any apical 'ballooning' but revealed features of an apical hypertrophic cardiomyopathy on cine images. Tissue characterization with T2 weighted images proved severe edema as the cause of significantly increased apical wall thickness. A follow-up cardiovascular magnetic resonance study was performed 5 months later which showed that edema, wall thickening and the appearance of apical hypertrophic cardiomyopathy all resolved, confirming Takotsubo syndrome as the cause of the initial appearance. As the affected myocardium most commonly involves the apical segments, an edema induced increase in apical wall thickness may lead to appearances of an apical hypertrophic cardiomyopathy rather than apical ballooning in the acute to subacute phase of Takotsubo syndrome.
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Left ventricular scanning by echocardiography and ultrasono-cardiotomography was performed to search the possible muscular abnormality in 9 cases with giant T wave inversion without documented cause. The deeply inverted T wave was more than 1.2mV (average was 1.63mV) in the left precordial leads. All the cases had electrocardiographic left ventricular hypertrophy of obscure origin and ischemic episode was absent. Conventional echo beam direction to measure the short axis of the left ventricle disclosed almost normal thickness and movement of both interventricular septum (IVS) and the posterior wall (PW), so that the report of these cases is frequently within normal limits. However, ultrasono-cardiotomography (sector B scan) disclosed the fairly localized hypertrophy near the left ventricular apex, and conventional echocardiography also revealed the same area of either IVS or PW or both below the insertion of the papillary muscles, when the scanning towards the apex was performed (asymmetrical apical hypertrophy: AAH).Control study of 9 cases with IHSS showed asymmetrical septal hypertrophy (ASH) with almost equally hypertrophied IVS from base to apex. All cases had inverted T waves, but these were of lesser degree. Three cases had relatively deep T wave compatible with those of AAH, and these cases also had the apical hypertrophy of considerable degree (unusual type of IHSS, i.e., intermediate type between AAH and ASH).The close relationship between the depth of the inverted T waves and the Apex/Mid wall thickness ratios suggests that the altered recovery process of the hypertrophied apical musculature is responsible for the giant T wave inversion of heretofore unsolved origin. Until the connective link of AAH to the other forms of hypertrophic cardiomyopathy is disclosed, the cases with such a T wave and the apical hypertrophy may be designated as asymmetrical apical hypertrophy (AAH).
In this report, we introduce a case of thickening of the involved left ventricular apical segment on echocardiography and deep T-wave inversions in precordial leads on electrocardiography transiently seen in the course of recovery from biventricular takotsubo cardiomyopathy, mimicking apical hypertrophic cardiomyopathy. This result suggests that the echocardiographic finding of transient myocardial edema can be identified by cardiac magnetic resonance imaging in takotsubo cardiomyopathy. Additionally, it persisted a few weeks after full functional recovery. We believe that this case will contribute in part toward clarifying the pathophysiology of takotsubo cardiomyopathy.
Apical akinesis and dilation in the absence of obstructive coronary artery disease is a typical feature of stress-induced (takotsubo) cardiomyopathy, whereas apical hypertrophy is seen in apical-variant hypertrophic cardiomyopathy. We report the cases of 2 patients who presented with takotsubo cardiomyopathy and were subsequently found to have apical-variant hypertrophic cardiomyopathy, after the apical ballooning from the takotsubo cardiomyopathy had resolved. The first patient, a 43-year-old woman with a history of alcohol abuse, presented with shortness of breath, electrocardiographic and echocardiographic features consistent with takotsubo cardiomyopathy, and no significant coronary artery disease. An echocardiogram 2 weeks later revealed a normal left ventricular ejection fraction and newly apparent apical hypertrophy. The 2nd patient, a 70-year-old woman with pancreatitis, presented with chest pain, apical akinesis, and a left ventricular ejection fraction of 0.39, consistent with takotsubo cardiomyopathy. One month later, her left ventricular ejection fraction was normal; however, hypertrophy of the left ventricular apex was newly noted. To our knowledge, these are the first reported cases in which apical-variant hypertrophic cardiomyopathy was masked by apical ballooning from stress-induced cardiomyopathy.
We report here the case of a 30-year-old professional soccer player who presented to our hospital after sustaining a blunt chest trauma. To the best of our knowledge, this is the first reported case of cardiac contusion when acute myocardial edema and subsequent chronic myocardial injury were visualized with cardiac magnetic resonance (CMR) imaging.
A professional soccer player presented to our hospital with persistent chest pain and fatigue after being hit in the chest by a soccer ball during a national league game. The hospital admission was 10 hours after the accident and onset of symptoms. The patient had no medical history and no recent history of infectious disease. The initial workup revealed elevated cardiac troponin T of 0.576 μg/L (normal range, 0.00 to 0.03 μg/L) and creatine kinase-MB levels of 25.4 U/L (normal range, 0 to 25 U/L); the markers of inflammation proved to be negative (C-reactive protein level, 0.9 mg/L [normal range, 0 to 5.0 mg/L]; white blood cell count, 7.0×103/μL [normal range, 4 to 10×103/μL]). The patient underwent a performance-enhancing drug screening 8 days before the event as part of the regular doping control protocol of professional soccer players, which proved to be negative. Furthermore, the toxicology panel testing for 7 drugs (phencyclidine, barbiturates, cannabinoids, amphetamines, benzodiazepines, …
Left ventricular scanning by echocardiography and ultrasono-cardiotomography was performed to search the possible muscular abnormality in 9 cases with giant T wave inversion without documented cause. The deeply inverted T wave was more than 1.2 mV (average was 1.63 mV) in the left precordial leads. All the cases had electrocardiographic left ventricular hypertrophy of obscure origin and ischemic episode was absent. Conventional echo beam direction to measure the short axis of the left ventricle disclosed almost normal thickness and movement of both interventricular septum (IVS) and the posterior wasll (PW), so that the report of these cases is frequently within normal limits. However, ultrasono-cardiotomography (sector B scan) disclosed the fairly localized hypertrophy near the left ventricular apex, and conventional echocardiography also revealed the same area of either IVS or PW or both below the insertion of the papillary muscles, when the scanning towards the apex was performed (asymmetrical apical hypertrophy: AAH). Control study of 9 cases with IHSS showed asymmetrical septal hypertrophy (ASH) with almost equally hypertrophied IVS from base to apex. All cases had inverted T waves, but these were of lesser degree. Three cases had relatively deep T wave compatible with those of AAH, and these cases also had the apical hypertrophy of considerable degree (unusual type of IHSS, i.e., intermediate type between AAH and ASH). The close relationship between the depth of the inverted T waves and the Apex/Mid wall thickness ratios suggests that the altered recovery process of the hypertrophied apical musculature is responsible for the giant T wave inversion of heretofore unsolved origin. Until the connective link of AAH to the other forms of hypertrophic cardiomyopathy is disclosed, the cases with such a T wave and the apical hypertrophy may be designated as asymmetrical apical hypertrophy (AAH).
In 30 of 1,002 consecutive patients who had left heart catheterization and cineangiography for evaluation of either ischemic heart disease or cardiomyopathy the electrocardiogram showed giant negative T waves (greater than 10 mm) associated with high QRS voltage (R wave greater than 26 mm in lead V5 or the sum of the S wave in lead V1 and the R wave in lead V5 35 mm or more) in the precordial leads despite absence of hypertension or significant coronary artery disease. In all 30 patients a characteristic spade-like configuration (concentric apical hypertrophy) was observed in the right anterior oblique ventriculogram at end-diastole as well as in the long axis two dimensional echocardiogram.
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