Diagnostic opportunities of magnetic resonant imagingmri of heart in differential diagnosis of phenotypical forms of hypertrophic cardiomyopathy

Introduction. Phenotype variants of left ventricular (LV) remodeling in patients with hypertrophic cardiomyopathy (HCM) are often associated with abnormalities of the mitral valve (MV), myocardiumstructure, contributing to the development of medium and/or subaortic obstruction. Itcauses the detail visualization of morphological obstruction substrates, tissue characteristics.Aim. To evaluate the possibilities of magnetic resonance imaging (MRI) in the diagnosis of various forms of HCM and combined abnormalities.Materials and methods. 75 patients with suspected HCM were examined. For verification, all patients underwentMRI using protocol: short-pulse T1w-TSE/ T2w-TSE (STIR), gradient echo in cine (CINE), T1-weighted post-contrast images (Inversion Recovery IR-MDE). Results. Patients classified into 4 types according to the anatomical principle (Wiggle E.D. et al., 1985). In addition to the most frequent forms affecting the interventricular septum (IVS) — 64 patients, unusual forms covering the apical zones and papillary muscles — 11 patients. The majority of patients were diagnosed with abnormalities of MV, divided into abnormalities of the number and position of papillary muscles, as well as the ratio of chords and muscles. Myocardial crypts were diagnosed in 12 patients, some combined with areas of non-compact myocardium. Post-contrast visualization using the delayed contrast technique allowed differentiating HCM with accumulation diseases, excluding cavity thrombosis, and evaluating the severity of myocardial fibrosis.Conclusions. MRI allows to estimate in details anatomic picture of LV remodeling, to diagnose features of the mitral valve, tissue characteristics that allows to stratify risk of sudden death, classify the HCM phenotype form and to determine the volume of surgical intervention.

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An Unusual Presentation of a Myocardial Crypt in Hypertrophic Cardiomyopathy

Case Reports in Cardiology ◽

10.1155/2014/737052 ◽

2014 ◽

Vol 2014 ◽

pp. 1-3

Author(s):

Danny A. J. P. van de Sande ◽

Jan Hoogsteen ◽

Luc J. H. J. Theunissen

Keyword(s):

Hypertrophic Cardiomyopathy ◽

Interventricular Septum ◽

Positive Family History ◽

Phenotypic Expression ◽

Anterior Wall ◽

Left Ventricular ◽

Genes Encoding ◽

History Of ◽

Basal Septum ◽

Myocardial Crypts

Hypertrophic cardiomyopathy (HCM) is a common inherited cardiovascular disease with prevalence of 0.2% in the population. More than 1000 mutations in more than 10 genes encoding for proteins of the cardiac sarcomere have been identified. Cardiac magnetic resonance imaging (CMR) is used to characterize left ventricular morphology with great precision in patients with HCM and it identifies unique structural abnormalities in patients with HCM. We present a case of a 56-year-old man who had positive family history of HCM who was a carrier of the genetic MYH-7 2770 G > C, exon 23 mutation. Transthoracic echocardiography showed thickening of the interventricular septum (16 mm) and in particular the basal septum. CMR confirmed the diagnosis of HCM in the anteroseptal myocardium with a thickness of 23 mm and also revealed large and deep myocardial crypts in the anterior wall. These myocardial crypts are rarely found in the so-called genotype positive and phenotype positive patients, as in our case. Also the crypts in this case are deeper and wider than those reported in other cases. So in conclusion, this case reveals an uncommon finding of a myocardial crypt at an unusual myocardial site with the unusual morphology in a patient with genotypic and phenotypic expression of hypertrophic cardiomyopathy.

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Membranous septal aneurysm in a child with Noonan syndrome and hypertrophic cardiomyopathy

10.22541/au.161496450.06346078/v1 ◽

2021 ◽

Author(s):

PRIYADARSHINI ARUNAKUMAR ◽

Usha MK ◽

RAMYA S ◽

Jayaranganath M

Keyword(s):

Hypertrophic Cardiomyopathy ◽

Mitral Valve ◽

Noonan Syndrome ◽

Left Ventricular Outflow Tract ◽

Interventricular Septum ◽

Ventricular Outflow Tract ◽

Left Ventricular ◽

Outflow Tract ◽

Mitral Leaflet ◽

Left Ventricular Outflow

A four year old boy was diagnosed with hypertrophic cardiomyopathy with moderate degree of obstruction of the left ventricular outflow tract, secondary to asymmetric septal hypertrophy and no features of congestive heart failure, at the age of the 7 months. He was also found to have myxomatous mitral valve, systolic anterior motion of anterior mitral leaflet and moderate mitral regurgitation. There was no evidence of ventricular septal defect at this point in time.In view of phenotypic features suggestive of Noonan syndrome, he underwent genetic evaluation with target gene sequencing and was detected to have a novel heterozygous mutation in exon 13 of LZTR 1 (Leucine- zipper-like transcriptional regulator 1) gene. Echocardiogram on follow up showed increase in left ventricular outflow tract obstruction and appearance of an aneurysm in the membranous portion of interventricular septum. There were no features of right ventricular outflow obstruction, tricuspid regurgitation or aortic regurgitation. The appearance of the membranous septal aneurysm may be related to the direction of jet arising from the point of contact of the anterior mitral leaflet with the hypertrophied basal septum and hitting this part of the interventricular septum. It is an unusual mechanism for formation of membranous septal aneurysm, given its absence in the earlier echocardiograms and absence of any left to right shunt across the aneurysm. He has been initiated on beta blockers due to severe left ventricular outflow tract obstruction and is planned for septal myomectomy, resection of membranous septal aneurysm and mitral valve repair.

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P1321 A case of multiple levels of ventricular obstruction

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jez319.762 ◽

2020 ◽

Vol 21 (Supplement_1) ◽

Author(s):

D Oikonomidis ◽

A Klitirinos ◽

M Koutouzis ◽

A Kalangos ◽

E Lazaris ◽

...

Keyword(s):

Hypertrophic Cardiomyopathy ◽

Mitral Valve ◽

Aortic Valve ◽

Interventricular Septum ◽

Left Ventricular ◽

Imaging Modalities ◽

Subaortic Stenosis ◽

Shortness Of Breath ◽

Septal Myectomy ◽

Subaortic Membrane

Abstract Subaortic stenosis (SAS) is a rare entity in adults with unclear etiology and variable presentation. SAS may be presented with symptoms mimicking Hypertrophic Cardiomyopathy (HCM). Often a combination of imaging modalities is needed to distinguish SAS from HCM with obstruction. A 53 years old man, smoker, was referred to our medical center suffering from shortness of breath on exertion. He first presented at another facility with a 2 month history of shortness of breath and chest discomfort during brisk physical activity and the possible diagnosis of HCM was made. On physical examination, a 3/6 systolic murmur was audible along the left sternal border, that became louder with standing and the Valsalva maneuver. The patient had non distended jugular veins, clear lung fields and no ankle edema. The results of laboratory exams did not reveal any pathological sign. The transthoracic echocardiogram revealed significant left ventricular hypertrophy (Interventricular septum 21 mm, Posterior wall 16 mm) with normal left ventricular systolic performance (ejection fraction >70%). The aortic valve was tricuspid and calcified whereas mitral valve was morphologically normal, with systolic anterior motion and mild posterolaterally directed regurgitation. Two systolic gradients, one dynamic, late peaking of 85mmHg and another fixed of 70mmHg were detected in left ventricular outflow track (LVOT). Transesophageal echocardiography was performed for the better evaluation of aortic valve and showed a three level obstruction caused by the systolic motion of the mitral valve towards the hypertrophic septum at LVOT, the presence of a membranous subaortic membrane and the calcified aortic valve respectively. The aortic valve was calcified with a moderate stenosis (0.8cm2 / m2) from 3D planimetry. A Cardiac Magnetic Resonance exam was ordered and confirmed the significance of hypertrophy and the presence of circumferential subaortic membrane. No late enhancement after the administration of Gadolinium was observed. Coronary angiography was performed and demonstrated normal coronary arteries. We hypothesized that the presence of subaortic membrane led to marked myocardial wall thickness and to the destruction of the aortic valve due to turbulent flow in the LVOT. The patient was referred for surgical management Extended septal myectomy combined with complete resection of orbital subaortic membrane were performed. he calcified aortic valve was replaced by bioprosthetic valve No 23mm. The patient tolerated the procedure well with significant symptomatic improvement. TTE performed 1 month postoperatively showed no remarkable LVOT gradient. The results of histopathology and genes investigations are pending. Subaortic membrane is a rare cause of symptoms that can mimic hypertrophic cardiomyopathy. A combination of imaging modalities is needed to distinguish subaortic stenosis from aortic valve stenosis and hypertrophic obstructive cardiomyopathy. Abstract P1321 Figure. Three levels obstruction

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The role of subvalvular structures in the development of mitral valve prolapse in children

Kazan medical journal ◽

10.17816/kmj1875 ◽

2012 ◽

Vol 93 (3) ◽

pp. 490-493

Author(s):

Yu M Belozerov ◽

Sh M Magomedova ◽

Z S Abakarova ◽

I M Osmanov

Keyword(s):

Mitral Valve ◽

Left Ventricle ◽

Mitral Valve Prolapse ◽

Interventricular Septum ◽

Left Ventricular ◽

Functional Mitral Regurgitation ◽

Healthy Children ◽

Papillary Muscles ◽

Functional Parameters

Aim. To assess the role of subvalvular structures in the development of mitral valve prolapse in children. Methods. Conducted was an echocardiography investigation with comparative analysis of structural and functional parameters of subvalvular structures in healthy children (50 individuals) and children with mitral valve prolapse divided in two groups: first group - without regurgitation (34 children), the second group - with regurgitation (16 children). Results. In healthy children identified were strong correlation links between echocardiographic indices of the subvalvular structures of the mitral valve and the functional parameters of the left ventricle. The diameter of the anterolateral group of papillary muscles directly correlated with the thickness of the interventricular septum, while the diastolic distance between the papillary muscles - with the end diastolic diameter of the left ventricle. It was established that the following factors may contribute to the pathogenesis of mitral valve prolapse: (1) long papillary muscles and the corresponding chords of the valve, (2) a weak (relative to the norm) contractile ability of the papillary muscles, (3) hyperkinesis of the left ventricular apex, and (4) no relationship between the apical and the global ejection fraction. These factors contribute to the fact that the papillary muscles and chords constrain the mitral valve cusps to a lesser extent during systole, which in turn easily bulge into the left atrium under the influence of systolic blood pressure. Apical hyperkinesis contributes to even closer approximation of the subvalvular structures with the cusps. Conclusion. Mitral valve prolapse is attributed to desynchronization of the function of papillary muscles and of the left ventricle; the development of functional mitral regurgitation during mitral valve prolapse is associated with dyssynchrony of the papillary muscles’ activity.

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Left ventricular reverse remodeling after successful subannular mitral valve repair in end-stage heart failure: a case report

European Heart Journal - Case Reports ◽

10.1093/ehjcr/ytaa087 ◽

2020 ◽

Vol 4 (3) ◽

pp. 1-5

Author(s):

Jonas Pausch ◽

Tatiana Sequeira Gross ◽

Hermann Reichenspurner ◽

Evaldas Girdauskas

Keyword(s):

Heart Failure ◽

Mitral Valve ◽

Mitral Regurgitation ◽

Mitral Valve Repair ◽

Left Ventricular ◽

Papillary Muscles ◽

Valve Repair ◽

Lv Remodeling ◽

End Stage Heart Failure ◽

End Stage

Abstract Background Due to ongoing left ventricular (LV) remodeling and consecutive geometric displacement of both papillary muscles, end-stage heart failure is frequently associated with relevant functional mitral regurgitation (FMR) Type IIIb. Treatment strategies of FMR and their prognostic impact are still controversial. Case summary We present a case of an 80-year-old patient who suffered from recurrent symptoms of congestive heart failure due to dilated cardiomyopathy and concomitant severe FMR. To specifically address severe tethering of both mitral leaflets heart team decision was to perform minimally invasive mitral valve repair (MVR) including a subannular LV remodeling procedure, instead of an interventional edge-to-edge repair (MitraClip® procedure). In addition to mitral valve ring annuloplasty, standardized relocation of both papillary muscles was performed successfully, leading to a complete resolution of mitral leaflet tethering. There were no procedural complications and the patient was discharged with an excellent functional result without residual mitral regurgitation. Furthermore, after 12 and 24 months, he reported an increase of his functional exercise capacity and a remarkable reverse LV remodeling could be demonstrated. Discussion Novel subannular repair techniques, especially the relocation of both papillary muscles, specifically address severe leaflet tethering in FMR and have an obvious potential to improve long-term competence of MVR. Therefore, they could be considered as a viable therapeutic option even in elderly patients presenting with end-stage cardiomyopathy and severe leaflet tenting.

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Early Clinical Results After Stentless Mitral Valve Implantation and Comparison With Conventional Valve Repair or Replacement

Circulation ◽

10.1161/circ.100.suppl_2.ii-78 ◽

1999 ◽

Vol 100 (suppl_2) ◽

Author(s):

Thomas Walther ◽

Claudia Walther ◽

Volkmar Falk ◽

Anno Diegeler ◽

Ralf Krakor ◽

...

Keyword(s):

Mitral Valve ◽

Valve Replacement ◽

Mitral Valve Replacement ◽

Maximum Flow ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Papillary Muscles ◽

Valve Repair ◽

Promising Alternative ◽

Ventricular Ejection Fraction

Background —A new quadricusp stentless mitral bioprosthetic valve (QMV) is evaluated and compared with current standards. Methods and Results —Since August 1997, 67 patients were prospectively evaluated: 23 patients received a QMV, 23 had mitral valve repair (MVR), and 21 received conventional mitral valve replacement (MVP). Patient age was 69±8, 64±10, and 62±9 years for QMV, MVR, and MVP treatment, respectively. The underlying pathology was mitral stenosis, incompetence, and mixed disease in a corresponding 8, 9, and 6 patients for QMV, 1, 22, and 0 patients for MVR, and 2, 12, and 7 patients for MVP. The papillary muscles were sufficient in all QMV cases to suspend the valve. Cross-clamp time was 59±19 minutes for QMV implantation. In-hospital mortality for QMV, MVR, and MVP was 1, 0, and 0 patients, respectively, and thoracotomy had to be performed again in 1, 1, and 2 patients, respectively (these outcomes were not valve related). At baseline transthoracic echocardiography, respective maximum flow velocities were 1.6, 1.4, and 1.7 m/s, and valve orifice area was 2.6, 3.5, and 3.4 cm 2 . Mild transvalvular reflux was seen in 8, 7, and 2 patients; moderate reflux, in 1, 1, and 1 patients. Left ventricular ejection fraction was 52%, 54%, and 51% in the respective treatment groups. At follow-up, hemodynamic parameters had further improved in all groups. Conclusions —One year after clinical implantation, the QMV appears to function well and has no additional risks compared with MVR or MVP. The subvalvular apparatus is preserved by suspending the QMV at the papillary muscles; this arrangement is hemodynamically advantageous. Echocardiography reveals an excellent valve performance that resembles native mitral valve morphology and hemodynamic function. The QMV is a promising alternative for biological mitral valve replacement.

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Alcohol septal ablation in hypertrophic cardiomyopathy

Global Cardiology Science and Practice ◽

10.21542/gcsp.2018.30 ◽

2018 ◽

Vol 2018 (3) ◽

Author(s):

Juan José Santos Mateo ◽

Juan R Gimeno

Keyword(s):

Hypertrophic Cardiomyopathy ◽

Interventricular Septum ◽

Ventricular Outflow Tract ◽

Clinical Results ◽

Left Ventricular ◽

Alcohol Septal Ablation ◽

Obstructive Hypertrophic Cardiomyopathy ◽

Left Ventricular Outflow ◽

Surgical Myectomy

Alcohol septal ablation (ASA) has become an alternative to surgical myectomy in obstructive hypertrophic cardiomyopathy since it was first introduced in 1994 by Sigwart. The procedure alleviates symptoms by producing a limited infarction of the upper interventricular septum, resulting in a decrease in left ventricular outflow tract (LVOT) gradient. The technique has been improved over time and the results are comparable with those of myectomy. Initial concerns about long-term outcomes have been largely resolved. In this review, we discuss indications, technical aspects, clinical results and patient selection to ASA.

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P228 Mitral valve aneurysm in the context of post-infective endocarditis in hypertrophic cardiomyopathy: an issue of inflammation or pressure gradients?

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jez319.093 ◽

2020 ◽

Vol 21 (Supplement_1) ◽

Author(s):

I Pereira Oliveira ◽

D Seabra ◽

A Neto ◽

I Cruz ◽

G Abreu ◽

...

Keyword(s):

Case Report ◽

Infective Endocarditis ◽

Hypertrophic Cardiomyopathy ◽

Mitral Valve ◽

Late Complication ◽

Fatal Outcome ◽

Left Ventricular ◽

Pressure Gradients ◽

Optimal Approach

Abstract Mitral valve aneurysms (MVA) are uncommon and usually develop acutely in the setting of infective endocarditis (IE). We present a case report of a patient with a ruptured aneurysm of the mitral valve (MV) leaflet and obstructive hypertrophic cardiomyopathy (HCM), previously treated for IE. Echocardiography is essential for diagnosis, highlighting the importance of imaging for early identification and timely intervention. CASE REPORT 68-year-old male patient with type 2 diabetes mellitus and dyslipidemia was admitted to hospital with a 3-week history of malaise, fever and recent left-sided abdominal pain. No past relevant history. Physical examination revealed a grade II/VI systolic heart murmur at the cardiac apex, fever, abdominal tenderness in the left upper quadrant and purpuric lesions in the inferior limbs. Neutrophilia, CPR 211mg/L. Positive blood cultures for Staphylococcus aureus methicillin-sensitive. Spleen embolization, with no abcess on abdominal CT. Transthoracic (TTE) and transesophageal echocardiography (TEE) disclosed a highly mobile polypoid mass in the atrial side of the anterior MV leaflet, septal left ventricular hypertrophy and systolic anterior motion (SAM) of the MV. Mild mitral regurgitation (MR). No evidence of abcess, aneurysm or valve perforation. The diagnosis of IE was established and the patient completed 42 days of Flucloxaciline. Favorable clinical evolution, residual lesions on the MV. TTE and TEE were repeated on follow-up. Besides HCM and SAM of the MV, an aneurysm of the anterior leaflet of the MV was identified and two regurgitant jets: one due to incomplete coaptation of the leaflets; other through the perforated aneurysm. Mild global MR. A strategy of close follow-up was adopted. Beta blocker dose was increased. Maintenance of the characteristics of the aneurysm. DISCUSSION MVA are rare, with perforation and significant MR development as the most serious complications. They mostly develop in the acute setting of IE of the aortic valve (AV), due to the "jet lesion" from the regurgitant jet or direct extension of the infection. In this case, MVA developed as a late complication of IE of the MV. Previous infection and inflammation lead to increased susceptibility of the valve leaflet, with possible persistent chronic inflammation. In the setting of obstructive HCM, the lesioned endothelium is exposed to significant intraventricular pressure gradients, which have probably raised its propensity to bulge towards the atrium, resulting in aneurysm formation and perforation. Optimal approach to MVA has not been defined. If the setting of perforation with severe MR, surgery must be performed in order to avoid a fatal outcome. In small aneurysms with mild MR, a conservative approach seems reasonable. The purpose of this case is to highlight potential complications of IE, which should be actively investigated, with echocardiography playing a central role in the diagnosis and follow-up.

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Altered hemodynamics in transgenic mice harboring mutant tropomyosin linked to hypertrophic cardiomyopathy

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.5.h2414 ◽

2000 ◽

Vol 279 (5) ◽

pp. H2414-H2423 ◽

Cited By ~ 27

Author(s):

Christian C. Evans ◽

James R. Pena ◽

Ronald M. Phillips ◽

Mariappan Muthuchamy ◽

David F. Wieczorek ◽

...

Keyword(s):

Hypertrophic Cardiomyopathy ◽

Protein Kinase ◽

Left Ventricular ◽

Familial Hypertrophic Cardiomyopathy ◽

Fiber Bundles ◽

Papillary Muscles ◽

Adrenergic Stimulation ◽

Skinned Fiber Bundles ◽

Force Relationship ◽

Kinase A

We used transgenic (TG) mice overexpressing mutant α-tropomyosin [α-Tm(Asp175Asn)], linked to familial hypertrophic cardiomyopathy (FHC), to test the hypothesis that this mutation impairs cardiac function by altering the sensitivity of myofilaments to Ca2+. Left ventricular (LV) pressure was measured in anesthetized nontransgenic (NTG) and TG mice. In control conditions, LV relaxation was 6,970 ± 297 mmHg/s in NTG and 5,624 ± 392 mmHg/s in TG mice ( P < 0.05). During β-adrenergic stimulation, the rate of relaxation increased to 8,411 ± 323 mmHg/s in NTG and to 6,080 ± 413 mmHg/s in TG mice ( P < 0.05). We measured the pCa-force relationship (pCa = −log [Ca2+]) in skinned fiber bundles from LV papillary muscles of NTG and TG hearts. In control conditions, the Ca2+ concentration producing 50% maximal force (pCa50) was 5.77 ± 0.02 in NTG and 5.84 ± 0.01 in TG myofilament bundles ( P < 0.05). After protein kinase A-dependent phosphorylation, the pCa50 was 5.71 ± 0.01 in NTG and 5.77 ± 0.02 in TG myofilament bundles ( P < 0.05). Our results indicate that mutant α-Tm(Asp175Asn) increases myofilament Ca2+-sensitivity, which results in decreased relaxation rate and blunted response to β-adrenergic stimulation.

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P881 Young patient with left ventricular hypertrophy and accidentally discovered aortic dissection: hypertensive heart or hypertrophic cardiomyopathy?

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jez319.522 ◽

2020 ◽

Vol 21 (Supplement_1) ◽

Author(s):

M Gawor ◽

M Franaszczyk ◽

E Kowalik ◽

M Spiewak ◽

I Michalowska ◽

...

Keyword(s):

Chest Pain ◽

Hypertrophic Cardiomyopathy ◽

Aortic Dissection ◽

Troponin T ◽

Global Longitudinal Strain ◽

Interventricular Septum ◽

Positive Family History ◽

Left Ventricular ◽

Jugular Veins ◽

Rare Differential Diagnosis

Abstract A 36-year-old male with positive family history of sudden cardiac death (his uncle"s son died suddenly at the age of 25), hospitalized a month ago in a local hospital due to acute hypertensive cardiogenic pulmonary edema, was referred to our institution for further evaluation with suspicion of hypertrophic cardiomyopathy. On admission patient was asymptomatic, without fatigue, exertional dyspnoea, chest pain or syncope. On physical examination his BP was significantly elevated (180/100 mmHg). The lungs were clear on auscultation, liver was not enlarged, jugular veins were normal, there was no oedema of lower extremities. Abdominal auscultation revealed vascular murmur in umbilical region. The baseline level of NT-proBNP was 811.4 (range 0–125) pg/mL, and high-sensitivity cardiac troponin T was 20.2 (range 0–14) ng/L. The standard 12-lead electrocardiogram demonstrated sinus rhythm, left atrial enlargement and left ventricular (LV) hypertrophy with nonspecific ST segment and T-wave changes (Fig. 1A). No significant pathology was present on chest X-ray (Fig. 1B). Transthoracic echocardiography revealed significant concentric LV hypertrophy with preserved LV ejection fraction (EF 70%) and moderately decreased global longitudinal strain (GLS-13.7%). There was mild dilatation of left atrium. Ascending aorta diameter was in normal range (Fig. 1C-D). Cardiac magnetic resonance (CMR) scan confirmed concentric LV hypertrophy with the maximal wall thickness of 18 mm at interventricular septum, and increased myocardial mass (LV mass index 124 ml/m2, range 59–92). Moreover, small areas of late gadolinium enhancement were found in LV segments (Fig. 1E-F). Due to presence of vascular murmur in abdomen, ultrasound imaging was performed. The exam revealed abdominal aortic dissection (Fig. 1G-H). Patient was transferred to the computed tomography (CT) unit to confirm the diagnosis. Aortic dissection originated below renal arteries and involving common illiac arteries was detected (Stanford B). The presence of thrombi within the lumen created by the aortic dissection suggested chronic presentation. Patient was managed conservatively with strict blood pressure control and close follow up arranged. We decided to perform genetic analysis. Currently we are awaiting the results in hope that it will help us to establish the diagnosis and differentiate hypertensive heart from hypertrophic cardiomyopathy. In conclusion, aortic dissection typically presents with tearing chest pain and severe hemodynamic compromise. Painless dissection, like in this case, is relatively rare. Differential diagnosis between hypertensive heart and hypertrophic cardiomyopathy is crucial as it has direct therapeutic impact. Abstract P881 Figure 1

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