About obstructive HCM

HCM is commonly caused by sarcomere mutations, resulting in excess myosin-actin cross bridging and hypercontractility of the heart muscle^1,5,6

HCM is characterised by LV hypertrophy (≥15 mm) that cannot be explained by another cardiac or systemic disease^3,7–9

The estimated global prevalence of HCM is 1 in every 500 people, but the number of diagnosed cases is less than 1 in 3,000³

The majority of HCM cases are obstructive^3,9

Obstructive HCM occurs when the blockage caused by the thickened heart muscle substantially reduces blood flow out of the left ventricle, which is referred to as LVOT obstruction.^3,9

LVOT obstruction is defined by a peak LVOT gradient of ≥30 mmHg with or without provocation.^7,9

^~75%

of patients with HCM have LVOT obstruction, either with
provocation or at rest⁹

Variable disease presentation and non-specific symptoms can make diagnosing obstructive HCM difficult^3,10

Patients with obstructive HCM may experience a wide range of debilitating symptoms:³

Fatigue

Chest pain

Breathlessness

Palpitations

Dizziness

Syncope

Obstructive HCM can increase the risk of experiencing serious complications:^1,11,12

Heart failure

Atrial fibrillation

Stroke

Sudden cardiac death
(<1% of patients)

Current pharmacological therapies (such as beta blockers and calcium channel blockers) used for treating obstructive HCM offer a variable degree of symptomatic relief and do not address the underlying cause of the disease^5,13
Septal reduction therapies are complex invasive procedures that may carry important risks to patients and may result in irreversible
poor outcomes^5,13

Patients with symptomatic obstructive HCM suffer from reduced quality of life compared with the general population^4,14

Explore the current treatment landscape in obstructive HCM

HCM, hypertrophic cardiomyopathy; LV, left ventricular; LVOT, left ventricular outflow tract.

References

Ho CY et al. Circulation. 2018;138(14):1387–1398.
Olivotto I et al. Circ Heart Fail. 2012;5(4):535–546.
Zaiser E et al. J Patient Rep Outcomes. 2020;4(1):102.
Capota R et al. Health Qual Life Outcomes. 2020;18(1):351.
Olivotto I et al. Lancet. 2020;396(10253):759–769.
Marian AJ, Braunwald E. Circ Res. 2017;121(7):749–770.
Arbelo E et al. Eur Heart J. 2023;44(37):3503–3626.
Pantazis A et al. Echo Res Pract. 2015;2(1):R45–R53.
Ommen SR et al. Circulation. 2020;142(25):e558–e631.
Argulian E et al. Am J Med. 2016;129(2):148–152.
Maron BJ et al. J Am Coll Cardiol. 2002;39(2):301–307.
O’Mahony C et al. Circ Arrhythm Electrophysiol. 2013;6(2):443–451.
Desai N et al. Clin Ther. 2022;44(1):52–66.
Magnusson P et al. Health Qual Life Outcomes. 2016;14:62.

HCM is commonly caused by sarcomere mutations, resulting in excess myosin-actin cross bridging and hypercontractility of the heart muscle1,5,6

HCM is characterised by LV hypertrophy (≥15 mm) that cannot be explained by another cardiac or systemic disease3,7–9

The estimated global prevalence of HCM is 1 in every 500 people, but the number of diagnosed cases is less than 1 in 3,0003

Explore the current treatment landscape in obstructive HCM

References

HCM is commonly caused by sarcomere mutations, resulting in excess myosin-actin cross bridging and hypercontractility of the heart muscle^1,5,6

HCM is characterised by LV hypertrophy (≥15 mm) that cannot be explained by another cardiac or systemic disease^3,7–9

The estimated global prevalence of HCM is 1 in every 500 people, but the number of diagnosed cases is less than 1 in 3,000³