Invasive Assessment of Microvascular Resistance in Hypertrophic Cardiomyopathy With Echocardiographic Correlates

Bakar, Shahrukh N.; Hayman, S.; McCarty, David; Thain, Andrew; McLellan, Andrew; Wagner, Cassandra; Lavi, Shahar

doi:10.1016/j.hlc.2021.07.002

Cited by 4 publications

(2 citation statements)

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“…The pathophysiological features of HCM are: cardiomyocyte hypertrophy [ 77 , 78 , 79 , 80 ] and disarray [ 78 , 79 , 80 , 81 ], myocardial remodeling [ 79 , 82 , 83 ] and fibrosis [ 1 , 24 , 79 , 84 , 85 , 86 ], coronary microvascular dysfunction [ 20 , 79 , 80 , 87 , 88 ], myocardial ischemia [ 20 , 79 , 88 , 89 , 90 ] and hypercontractility [ 8 , 79 , 91 , 92 , 93 ], impaired myocardial relaxation [ 8 , 79 , 84 , 94 ], myocardial stiffness [ 79 , 81 , 84 ], and diastolic dysfunction [ 79 , 81 , 95 , 96 ].…”

Section: Outcomes Of Hcmmentioning

confidence: 99%

“…Some patients are completely asymptomatic [ 1 , 2 , 3 , 80 , 116 ] and can be identified incidentally [ 1 ], while others manifest LV outflow tract obstruction (LVOTO) [ 18 , 79 , 90 , 93 , 115 , 116 ], atrial fibrillation (AF) [ 1 , 9 , 79 , 115 ], SCD [ 1 , 2 , 6 , 79 , 116 , 117 ], or HF [ 1 , 3 , 5 , 6 , 79 , 118 ]. Most HCM cases remain asymptomatic or mildly symptomatic throughout their life [ 73 ], whereas others experience chest pain, fatigue, (exertional) dyspnea, palpitations, presyncope, and syncope [ 1 , 8 , 20 , 44 , 73 , 88 , 119 , 120 , 121 ], with dyspnea being the most common and syncope the least common [ 119 ]. The frequency of dyspnea and palpitations increases with age [ 73 ].…”

Section: Outcomes Of Hcmmentioning

confidence: 99%

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Hypertrophic Cardiomyopathy: Genetic Foundations, Outcomes, Interconnections, and Their Modifiers

2023

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Hypertrophic cardiomyopathy (HCM) is the most prevalent heritable cardiomyopathy. HCM is considered to be caused by mutations in cardiac sarcomeric protein genes. Recent research suggests that the genetic foundation of HCM is much more complex than originally postulated. The clinical presentations of HCM are very variable. Some mutation carriers remain asymptomatic, while others develop severe HCM, terminal heart failure, or sudden cardiac death. Heterogeneity regarding both genetic mutations and the clinical course of HCM hinders the establishment of universal genotype–phenotype correlations. However, some trends have been identified. The presence of a mutation in some genes encoding sarcomeric proteins is associated with earlier HCM onset, more severe left ventricular hypertrophy, and worse clinical outcomes. There is a diversity in the mechanisms implicated in the pathogenesis of HCM. They may be classified into groups, but they are interrelated. The lack of known supplementary elements that control the progression of HCM indicates that molecular mechanisms that exist between genotype and clinical presentations may be crucial. Secondary molecular changes in pathways implicated in HCM pathogenesis, post-translational protein modifications, and epigenetic factors affect HCM phenotypes. Cardiac loading conditions, exercise, hypertension, diet, alcohol consumption, microbial infection, obstructive sleep apnea, obesity, and environmental factors are non-molecular aspects that change the HCM phenotype. Many mechanisms are implicated in the course of HCM. They are mostly interconnected and contribute to some extent to final outcomes.

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