Stress Hypoperfusion and Tissue Injury in Hypertrophic Cardiomyopathy

Abstract

Background— Ischemia and tissue injury are common in patients with hypertrophic cardiomyopathy. Cardiovascular magnetic resonance imaging offers combined evaluations of each phenomenon at sufficiently high resolution to examine transmural spatial distribution. In this prospective cohort study, we examine the spatial distribution of stress perfusion abnormalities and tissue injury in patients with hypertrophic cardiomyopathy. Methods and Results— One hundred consecutive patients with hypertrophic cardiomyopathy underwent cardiovascular magnetic resonance imaging. Cine, stress perfusion, late gadolinium enhancement, and T2-weighted imaging techniques were used. Each was spatially coregistered according to predefined segmental and subsegmental models and was blindly analyzed for abnormalities using validated techniques. Spatial associations among stress perfusion, late gadolinium enhancement, and T2 imaging were made at segmental and subsegmental levels. Of the 100 patients studied, the phenotype was septal in 86 and apical in 14. Late gadolinium enhancement imaging was abnormal in 79 patients (79%). Eighty-six patients met prespecified safety criteria to undergo stress perfusion, and ischemia was identified in 46 patients (57%). T2 imaging was available in 81 patients and was abnormal in 19 (29%). The dominant distribution of all 3 findings was to segment with hypertrophy. Subsegmental analysis revealed geographic dominance of ischemia within the subendocardial zones. However, this zone was most commonly spared from late gadolinium enhancement and T2 abnormalities, typically seen in midwall and subepicardial zones. Conclusions— Inducible hypoperfusion is a common finding in hypertrophic cardiomyopathy and is typically identified within segments exhibiting imaging markers of tissue injury. However, the respective transmural dominance of these phenomena seems distinct. Alternate factors contributing to a regional susceptibility to tissue injury are deserving of further study.

Coronary microvascular ischemia in hypertrophic cardiomyopathy - a pixel-wise quantitative cardiovascular magnetic resonance perfusion study

“…On histology, Varnava et al found a poor interrelationship between myocardial fibrosis, small vessel disease and disarray [16]. These findings are also in accord with those of Tyan et al who semi-quantitatively assessed the distribution of perfusion abnormalities and tissue injury using CMR [42]. The absence of a dose–response relationship between reduced hyperemic MBF and the observed spatial distribution of LGE suggests that factors other than or beyond ischemia must be implicated in the pathogenesis of replacement fibrosis in HCM.…”

Cardiac Magnetic Resonance Myocardial Perfusion Reserve Index Is Reduced in Women With Coronary Microvascular Dysfunction

“…Impairment of myocardial perfusion reserve has also been documented in some asymptomatic individuals with multiple cardiac risk factors in the Multi-Ethnic Study of Atherosclerosis, in asymptomatic patients with hypertrophic cardiomyopathy and in women with chest pain and systemic lupus erythematosus 10, 17 . A variety of CMRI techniques have been reported in single center studies of small groups of patients and these vary widely in terms of technical complexity, clinical applicability and system field strength (3.0T vs. 1.5T).…”

MR Imaging in Hypertrophic Cardiomyopathy: From Magnet to Bedside

“…Though a great deal of our knowledge regarding microvascular ischemia in HCM should be credited to the use of SPECT and PET, MR imaging has now become an interesting alternative (21,81) because of its superior spatial resolution and its capability to help identify myocardial fibrosis (Table 3) (Fig 11) (Movie 5 [online]) (82)(83)(84). The perfusion MR sequences do not differ from those used in patients with coronary artery disease (eg, saturation-recovery fast gradientecho sequence).…”

“…A decade later, it is fair to say that several gaps remain in our knowledge (94). We have learned that LGE is a common finding occurring in the majority of HCM patients (range, 33%-79%) with highly variable extent and intensity (83,95) and, consistent with prior pathologic studies, preferentially localized to the midwall of regions with maximum LV wall thickness (Table 1) (70,96,97). Stress-perfusion defects are often found in the same regions expressing LGE, although typically located in the subendocardial region rather than at midwall (Fig 11).…”

“…Stress-perfusion defects are often found in the same regions expressing LGE, although typically located in the subendocardial region rather than at midwall (Fig 11). However, LGE may also be observed in HCM hearts with no evidence of microvascular ischemia (82)(83)(84).…”