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Fulltext Native T1 and T2 provide distinctive signatures in hypertrophic cardiac conditions - Comparison of uremic, hypertensive and hypertrophic cardiomyopathy

Arcari L, Hinojar R, Engel J, Freiwald T, Platschek S, Zainal H, et al.

Int J Cardiol, 2020 05 01;306:102-108.
PMID: 32169347 DOI: 10.1016/j.ijcard.2020.03.002

AIMS: Profound left ventricular (LV) hypertrophy with diastolic dysfunction and heart failure is the cardinal manifestation of heart remodelling in chronic kidney disease (CKD). Previous studies related increased T1 mapping values in CKD with diffuse fibrosis. Native T1 is a non-specific readout that may also relate to increased intramyocardial fluid. We examined concomitant T1 and T2 mapping signatures and undertook comparisons with other hypertrophic conditions.
METHODS: In this prospective multicentre study, consecutive CKD patients (n = 154) undergoing routine clinical cardiac magnetic resonance (CMR) imaging were compared with patients with hypertensive (HTN, n = 163) and hypertrophic cardiomyopathy (HCM, n = 158), and normotensive controls (n = 133).
RESULTS: Native T1 was significantly higher in all patient groups, whereas native T2 in CKD only (p 

Matched MeSH terms: Hypertrophy, Left Ventricular/pathology
Cardiac sarcoidosis: two cases with autopsy findings

Wan Muhaizan WM, Swaminathan M, Daud MS

Malays J Pathol, 2004 Jun;26(1):59-63.
PMID: 16196153

Cardiac sarcoidosis is a disease of young adults. In most cases it presents with sudden death, arrhythmias, conduction disorders, heart failure or cardiomyopathy. The authors describe two cases of myocardial involvement by sarcoidosis that lead to death of the patients. Case one was a 26-year-old Indian man who was previously well and presented with sudden death. Autopsy showed nodules of sarcoid granuloma involving the heart, lungs and lymph nodes. Case two was a 47-year-old Indian lady who complained of reduced effort tolerance. Echocardiography showed that she had restrictive hypertrophic cardiomyopathy with heart failure. Seven months after initial presentation, she developed worsening of heart failure and died. Autopsy revealed involvement of the heart, lungs and liver by sarcoidosis.

Matched MeSH terms: Hypertrophy, Left Ventricular/pathology
Effect of captopril on urinary kallikrein, blood pressure and myocardial hypertrophy in diabetic spontaneously hypertensive rats

Sharma JN, Kesavarao U

Pharmacology, 2002 Apr;64(4):196-200.
PMID: 11893900 DOI: 10.1159/000056171

We investigated the total urinary kallikrein levels, left-ventricular wall thickness and mean arterial blood pressure of nontreated and captopril-treated diabetic and nondiabetic spontaneously hypertensive rats. The mean arterial blood pressure was significantly elevated in diabetic spontaneously hypertensive rats as compared to nondiabetic spontaneously hypertensive rats. Captopril treatment caused a significant reduction in the arterial blood pressure of both nondiabetic and diabetic spontaneously hypertensive rats. The left-ventricular wall thickness was also significantly reduced in diabetic and nondiabetic spontaneously hypertensive treated with captopril as compared to nontreated diabetic and nondiabetic spontaneously hypertensive rats. The total urinary kallikrein levels were significantly raised in captopril-treated diabetic and nondiabetic spontaneously hypertensive rats against the values obtained from nontreated diabetic and nondiabetic spontaneously hypertensive rats. These results indicate that blood pressure reduction and left ventricular wall regression with captopril treatment might be due to enhanced renal kallikrein formation. The significance of these findings is discussed.

Matched MeSH terms: Hypertrophy, Left Ventricular/pathology

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