The study aimed to determine if selenium deficiency, serum ceruloplasmin and traditional birth practices are risk factors for peripartum cardiomyopathy (PPCM), in Kano, Nigeria. This is a case-control study carried out in three hospitals, and PPCM patients were followed up for six months. Critically low serum selenium concentration was defined as <70 µg/L. A total of 39 PPCM patients and 50 controls were consecutively recruited after satisfying the inclusion criteria. Mean serum selenium in patients (61.7 ± 14.9 µg/L) was significantly lower than in controls (118.4 ± 45.6 µg/L) (p < 0.001). The prevalence of serum selenium <70 µg/L was significantly higher among patients (76.9%) than controls (22.0%) (p < 0.001). The mean ceruloplasmin and prevalence of socio-economic indices, multiparity, pregnancy-induced hypertension, obesity and twin pregnancy were not different between the groups (p > 0.05). Logistic regression showed that rural residency significantly increased the odds for serum selenium <70 µg/L by 2.773-fold (p = 0.037). Baseline serum levels of selenium and ceruloplasmin were not associated with six-month mortality. This study has shown that selenium deficiency is a risk factor for PPCM in Kano, Nigeria, and is related to rural residency. However, serum ceruloplasmin, customary birth practices and some other characteristics were not associated with PPCM in the study area.

The literature on right ventricular systolic dysfunction (RVSD) in peripartum cardiomyopathy (PPCM) patients is scanty, and it appears that RV reverse remodelling in PPCM has not been previously described. This study thus aimed to assess RVSD and remodelling in a cohort of PPCM patients in Kano, Nigeria. A longitudinal study carried out in 3 referral hospitals in Kano, Nigeria. Consecutive PPCM patients who had satisfied the inclusion criteria were recruited and followed up for 12 months. RVSD was defined as the presence of either tricuspid annular plane systolic excursion (TAPSE) <16 mm or peak systolic wave (S’) tissue Doppler velocity of RV free wall 0.05). RVSD and reverse remodelling were common in Nigerians with PPCM, in whom the first 6 months after diagnosis seem to be critical for RV recovery and survival.

The common pathophysiology contributing to fluid retention and dyspnoea in heart failure is a non-compliant and stiff myocardium with raised left ventricular end-diastolic pressure. With the rapid development of newer imaging technologies, particularly echocardiography, our understanding of the syndrome of heart failure has significantly changed. The most important imaging sign in the early eighties was reduced ejection fraction (HFrEF), with low values being used as an explanation for the development of signs and symptoms. In the early 2000s, similar Doppler echocardiographic signs became frequently recognised in patients with heart failure symptoms and signs who proved to have a relatively maintained ejection fraction (EF) of >40%, hence the description of the syndrome of “diastolic heart failure”. This was later rephrased as heart failure with normal ejection fraction (HFnEF) and more recently as heart failure with preserved ejection fraction (HFpEF). Since then, HFpEF has attracted the interest of many cardiologists and scientists worldwide, searching for specific features and treatment options for the syndrome. As for the features, two important findings have now been established, the first showed that LV systolic function mainly at the subendocardial level was abnormal in HFpEF, particularly manifesting during stress/exercise when the increase in heart rate was not associated with a commensurate increase in stroke volume and a second observation of a significant impairment of left atrial function (i.e. myocardial strain) and emptying fraction associated with increased left atrial pressures and the potential development of atrial arrhythmia in HFpEF. Such atrial abnormalities have been shown to be commonly associated with cavity enlargement and poor compliance. The latter observation has similarly been reported in patients with reduced EF. Despite the above similarities in cardiac physiology between HFpEF and HFrEF, treatments of the two conditions differ markedly. When comparing HFrEF and HFpEF, we can easily see that some patients fall into the grey area on the EF spectrum with values fluctuating above and below 40%, suggesting that the substrate for the expected drug effect may differ, possibly explaining the lack of consistent response in these patients.. In addition, it should not be forgotten that most heart failure medications work on the circulation rather than the heart itself, hence the need for shared circulatory disturbances between the two conditions before we can reasonably expect identical treatment benefits when using the same medications in different clinical settings. Therefore, it is clear that classifying heart failure patients according to a single measure of LV function i.e. ejection fraction fails to help at least 50% of patients presenting with this syndrome. In contrast, aggregating such patients based on clear evidence for raised LA pressures, irrespective of EF, might show evidence for a more consistent response to vasodilators and conventional heart failure therapy, particularly those patients currently described as HFpEF.