scholarly journals Apical Hypertrophic Cardiomyopathy and Myocardial Infarction in a Young Adult, a Rare Combination

2013 ◽  
Vol 14 (1) ◽  
pp. 74-76
Author(s):  
Gautam Datta ◽  
Dipankar Mukherjee ◽  
DM Bhubanmajhi ◽  
Rupesh Singh ◽  
Sudhir Bhattacharya

A teenage boy of 19 years without traditional risk factors for coronary artery disease, presented with typical anginal pain with ST-T changes in anterior leads and elevated cardiac troponin T. Investigation revealed the patient havingapical hypertrophic cardiomyopathy with normal coronary angiography and a spade shaped apex on LV angiography. With a diagnosis of microvascular infraction, further investigations revealed elevated LP (a), serum homocysteineand low HDL probably playing a contributory role.DOI: http://dx.doi.org/10.3329/jom.v14i1.14557 J MEDICINE 2013; 14 : 74-76

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hang Liao ◽  
Huay Cheem Tan ◽  
Ziqiong Wang ◽  
Xiaoping Chen ◽  
Yong He ◽  
...  

Abstract Background This study was performed to investigate the clinical significance of combined evaluation of both coronary artery disease (CAD) and high-sensitivity cardiac troponin T (hs-cTnT) for prediction of major adverse cardiovascular events (MACEs) in patients with hypertrophic cardiomyopathy (HCM). Methods We performed clinical evaluations, including coronary artery imaging and hs-cTnT measurement, in 162 patients with HCM. Results The patients were followed up for a median period of 3.7 years (interquartile range 2.4–5.6 years; total of 632.3 person-years [PYs]), during which time MACEs occurred in 24 (14.8%) patients. The incidence of MACEs was 6.4 and 2.7 per 100 PYs for patients with CAD and normal coronary arteries, respectively; similarly, the incidence was 5.8 and 2.1 per 100 PYs in patients with an elevated hs-cTnT concentration (> 14.0 ng/L) and a normal hs-cTnT concentration, respectively. The multivariate analysis suggested that CAD and an elevated hs-cTnT concentration tended to be positively associated with MACEs. When the groups were allocated according to these two markers, the patients were divided into four groups, which further improved the predictive values. The incidence of MACEs was 10.4 per 100 PYs in the CAD and elevated hs-cTnT group, which was much higher than the incidence in all other groups (range, 2.0–3.5 per 100 PYs). With the normal coronary arteries and normal hs-cTnT group serving as a reference, the adjusted hazard ratio was 5.0 (95% confidence interval 1.0–23.8; P = 0.046) for the CAD and elevated hs-cTnT group. In addition, the subgroup analysis showed similar findings among the patients without severe CAD. Conclusions In patients with HCM, combined evaluation of both CAD and hs-cTnT might facilitate more reliable prediction of MACEs than evaluation of a single marker. These may serve as clinically useful markers to guide risk management.


Cardiology ◽  
2000 ◽  
Vol 93 (3) ◽  
pp. 155-162 ◽  
Author(s):  
Tong-Lang Lin ◽  
Sahoko Ichihara ◽  
Yoshiji Yamada ◽  
Tetsuo Nagasaka ◽  
Hitoshi Ishihara ◽  
...  

2017 ◽  
Vol 313 (6) ◽  
pp. H1180-H1189 ◽  
Author(s):  
Alexis V. Mickelson ◽  
Murali Chandra

The central region of cardiac troponin T (TnT) is important for modulating the dynamics of muscle length-mediated cross-bridge recruitment. Therefore, hypertrophic cardiomyopathy mutations in the central region may affect cross-bridge recruitment dynamics to alter myofilament Ca2+ sensitivity and length-dependent activation of cardiac myofilaments. Given the importance of the central region of TnT for cardiac contractile dynamics, we studied if hypertrophic cardiomyopathy-linked mutation (TnTR94H)-induced effects on contractile function would be differently modulated by sarcomere length (SL). Recombinant wild-type TnT (TnTWT) and the guinea pig analog of the human R94H mutation (TnTR95H) were reconstituted into detergent-skinned cardiac muscle fibers from guinea pigs. Steady-state and dynamic contractile measurements were made at short and long SLs (1.9 and 2.3 µm, respectively). Our results demonstrated that TnTR95H increased pCa50 (−log of free Ca2+ concentration) to a greater extent at short SL; TnTR95H increased pCa50 by 0.11 pCa units at short SL and 0.07 pCa units at long SL. The increase in pCa50 associated with an increase in SL from 1.9 to 2.3 µm (ΔpCa50) was attenuated nearly twofold in TnTR95H fibers; ΔpCa50 was 0.09 pCa units for TnTWT fibers but only 0.05 pCa units for TnTR95H fibers. The SL dependency of rate constants of cross-bridge distortion dynamics and tension redevelopment was also blunted by TnTR95H. Collectively, our observations on the SL dependency of pCa50 and rate constants of cross-bridge distortion dynamics and tension redevelopment suggest that mechanisms underlying the length-dependent activation cardiac myofilaments are attenuated by TnTR95H. NEW & NOTEWORTHY Mutant cardiac troponin T (TnTR95H) differently affects myofilament Ca2+ sensitivity at short and long sarcomere length, indicating that mechanisms underlying length-dependent activation are altered by TnTR95H. TnTR95H enhances myofilament Ca2+ sensitivity to a greater extent at short sarcomere length, thus attenuating the length-dependent increase in myofilament Ca2+ sensitivity.


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