Table 3.

Investigations of patients with abnormal heart biomarkers and no history of heart disease or pulmonary arterial hypertension.

Age/sexBiomarkersECGTTEcMRIOutcome
74/FcTnI, BNP, CPKRBBB, LAFB, LQTLVH, RVH, LA, RA, IVSH, DD, LVEF = 30%LVH, RVH, LA, RA, IVSHHeart biopsy was pathognomonic for AMIC. AM discontinuation led to steady decrease of both cTnI and BNP and regression of hypertrophy.
63/FcTnI, BNP, CPKRBBB, LAFBLVH, RVH, LA, IVSH, DDLVH, RVH, LA, IVSH, LGE nonvascularHeart biopsy was pathognomonic for AMIC. AM discontinuation led to steady decrease of both cTnI and BNP and regression of hypertrophy.
74/FcTnI, BNP, CPKFirst-degree AVBLVH, LA, IVSH, DDLVH, RVH, LA, RA, IVSHNormal coronary angiography. Patient succumbed from refractory heart failure, complicated with septic shock. Possible AMIC.
59/FcTnI, BNPNormalLVH, IVSH, LA, RA, DDLVH, IVSHRegression of hypertrophy and decrease of heart biomarkers after 6 months. Possible AMIC.
49/FcTnI, BNP, CPKRBBBLVH, RVH, IVSH, LA, DDLVH, RVH, IVSH, LARegression of hypertrophy, all biomarkers normalized after 12 months. Possible AMIC.
67/FcTnI, BNP, CPKAtrial fibrillationLVH, LA, IVSH, DDLVH, IVSH, LAPossible AMIC, biomarkers at the same levels after 3 and 6 mos (AM not discontinued until later).
49/McTnI, BNPNormalLVH, LA, IVSH, DDNDCoronary artery disease (2 vessels), biomarkers unchanged after 6 mos (AM not discontinued).
57/FcTnI, BNP, CPKNonspecific T abnormalityLVH, IVSH, regional hypokinesis, LVEF = 55%LVH, LGE nonvascular, edemaMyocarditis. Treatment with cyclophosphamide and glucocorticoids led to regression of edema in cMRI. Partial decrease of biomarkers.
30/FBNPNormal, right axis deviationRVH, RVSP = 69 mmHgNDPH. Treatment with phosphodiesterase-5 inhibitors led to normalization of BNP after 6 mos.
38/FBNPNormalSmall pericardial effusion, RVSP = 44 mmHgNDPatient had nephrotic syndrome owing to active lupus nephritis. Elevated BNP was attributed to volume overload.
71/FBNPPossible LVH, incomplete RBBBLVHLVHUncontrolled hypertension. BNP remained at the same levels despite intensive treatment after 6 and 12 mos. Cardiac troponin was marginal and remained unchanged at the same time.
71/FBNPAtrial fibrillation, Possible LA enlargementLA enlargement, moderate MV regurgitationLA, LVHNo specific cause identified. BNP remained at the same levels after 6 months. AM dose was decreased.
44/FBNP, CPKPossible biatrial enlargementMild global hypokinesis of the LV, LVEF = 45%NDNo specific cause identified. Coronary CT with Agatston score 0. BNP remained in the same levels after 6 and 12 mos.
52/FBNPNormalNormalNormalNo specific cause identified. BNP remained in the same levels after 6 and 12 mos.
64/FBNP, CPKRBBB, possible LVHNormalNDNo specific cause identified. BNP remained in the same levels after 3, 6, and 12 mos.
48/McTnI, BNPNonspecific T abnormalityNormalNDNo specific cause identified. BNP and cTnI were slightly decreased (still abnormal) after 6, 9, and 12 mos
  • ECG: electrocardiogram; TTE: transthoracic echocardiogram; cMRI: cardiac magnetic resonance imaging; cTnI: cardiac troponin I; BNP: brain natriuretic peptide; CPK: creatine phosphokinase; RBBB: right bundle branch block; LAFB: left anterior fascicular block; LQT: long QT; LVH: left ventricular hypertrophy; RVH: right ventricular hypertrophy; LA: left atrium dilatation; RA: right atrium dilatation; IVSH: interventricular septum hypertrophy; LVEF: left ventricular ejection fraction; AM: antimalarials; AMIC: AM-induced cardiomyopathy; DD: diastolic dysfunction; LGE: late gadolinium enhancement; AVB: atrioventricular block; ND: not done; PH: pulmonary hypertension; RVSP: right ventricular systolic pressure; CT: computed tomography.