CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 4, September/October 2023 222 AFRICA Discussion The reported prevalence of RVSD in left HF varies with the stage and aetiology of the HF, as well as the definition of RVSD employed.14,15 The use of several indices of RV function, each measuring a different component of RV contractility, increases the chances of finding RVSD. The prevalence of RVSD was higher when assessed by the RV MPI than by TAPSE, RV S′ or RV FAC for all LVEF subgroups and all HF aetiologies. The RV MPI is said to be an index of global RV function that takes into account both systolic and diastolic RV function and appears to be independent of preload, afterload and heart rate.16 There was a significant association between the presence of RVSD and the degree of LV systolic and diastolic dysfunction. Experimental studies have suggested that approximately 20 to 40% of RV systolic function is contributed to by LV contraction through ventricular interdependence.4 In agreement with this, LVEF was independently associated with the presence of RVSD in the present study. Overall, an LVEF of < 40% was associated with a four-fold odds ratio (OR) of having RVSD (OR = 4.205, 95% CI: 1.643–10.760, p = 0.003). Similarly, RV systolic function worsened with worsening grade of LV diastolic function, with the prevalence of RVSD reaching 93.2% in those with a restrictive LV filling pattern. A mitral E/A > 2 was independently predictive of RVSD in the multivariable logistic regression analysis (OR = 4.684, 95% CI: 1.521–14.428, p = 0.007). RV systolic dysfunction was significantly more common in patients with non-hypertensive HF in the present study. Based on cut-off values generated from normal controls, an RVSD prevalence of as high as 81.6% was reported among patients with hypertensive HF in Ibadan, Nigeria.17 More normative studies are needed to define the limits of normal RV function in indigenous Africans. Ischaemic aetiology has been reported to be independently associated with a reduced TAPSE in patients with heart failure.18 Kjaergaard et al., in a study among Danish patients, found that patients with ischaemic cardiomyopathy had lower values of TAPSE compared to non-ischaemic aetiology (17 ± 5 vs 19 ± 5 mm, p = 0.001).19 However there is a suggestion that myocardial infarction involving the anterior wall of the left ventricle may produce an increased TAPSE as a compensatory response, while infarctions involving the right ventricle will produce a reduced TAPSE.20 In the present study, RV MPI was significantly higher (worse global RV function) in those with ischaemic heart disease. However, HF aetiology was not independently predictive of RVSD in the multivariable analysis. The presence of an elevated pulmonary pressure leading to afterload mismatch and contractile impairment has traditionally been considered a plausible cause for RV dysfunction in HF patients.21 The present study found that a PASP > 35 mmHg was associated with an increased odds of having of RVSD. This finding is consistent with our understanding of RV pulmonary artery coupling and the fact that RV function is highly afterload dependent.22 Consistent with that reported by Ghio et al. in a European population, the present study found that the independent association of a PASP > 35 mmHg with RVSD was significant, mainly in those with HFmrEF and HFpEF.18 The observation that RVSD was associated with the presence of an elevated RV afterload in HFpEF and HFmrEF is particularly important and provides a strong rationale for discovering effective treatments for pulmonary hypertension in such patients.23 However this association between RVSD and pulmonary pressure has not been consistently observed in other studies. The reason for this disparity is not immediately apparent but may be related to the varied aetiology of HF in the participants of the different studies, the definition of pulmonary hypertension and how it was measured. In our study, SBP had a significant correlation with all measures of RVSD and was independently predictive of RV FAC < 35% and RV S′ < 10 cm/s, mainly for those with HFrEF. The development of RVSD may result in the inability of the cardiovascular system to maintain an adequate blood pressure, even in those who were previously hypertensive. It is well known that in advanced heart failure, SBP is usually low, even in previously hypertensive patients.24 This phenomenon, which has been termed decapitated hypertension, occurs when patients who were previously hypertensive progressively develop normal and even low blood pressure as HF worsens.25 This decrease in SBP results from reduced pump function and a fall in cardiac output despite compensatory peripheral vasoconstriction.24 While hypertension is an established cause of incident HF, studies have shown that a higher SBP in patients with established heart failure seems to paradoxically have a protective effect on survival.26 On multivariate linear analysis, LVOT VTI, LAVI, RVOT diameter and LVEF demonstrated a significant relationship with Table 5. Cut-off values for LVOT VTI for the various measures of RVSD on ROC analysis AUC (95% CI) Cut-off value (cm) Sensitivity (%) Specificity (%) p-value RV FAC < 35% 0.882 (0.838–0.926) 9.8 81.5 81.9 < 0.001* TAPSE < 1.6 cm 0.834 (0.787–0.882) 11.4 74.5 71.2 < 0.001* RV S’ < 10 cm/s 0.832 (0.783–0.880) 10.3 77.1 70.2 < 0.001* RV MPI > 0.55 0.629 (0.547–0.708) 13.9 69.1 55.6 0.002* Total RVSD 0.779 (0.721–0.836) 13.6 73.9 68.7 < 0.001* AUC, area under the curve; CI, confidence interval; RV FAC, right ventricular fractional area change; TAPSE, tricuspid annular plane systolic excursion; RV S′, peak velocity of the tricuspid annulus in systole; RV MPI, right ventricular myocardial performance index; RVSD, right ventricular systolic dysfunction. *p-value is statistically significant. Table 6. Independent predictors of RVSD Predictors Univariate analysis Multivariate analysisa OR (95% CI) p-value Adjusted OR (95% CI) p-value MV E/A > 2 15.172 (6.200–37.127) < 0.001* 4.684 (1.521–14.428) 0.007* LVEF < 40% 10.107 (4.974–20.538) < 0.001* 4.205 (1.643–10.760) 0.003* PASP ≥ 35 mmHg 5.720 (2.830–11.562) < 0.001* 2.434 (1.012–5.852) 0.047* SBP < 140 mmHg 4.378 (2.445–7.836) < 0.001* 2.631 (1.152–6.011) 0.022* NYHA III/IV 5.056 (2.807–9.108) < 0.001* _ _ Male gender 1.020 (0.587–1.771) 0.945 _ _ Obesity 1.288 (0.620–2.678) 0.497 _ _ HR > 90 bpm 2.996 (1.694–5.299) < 0.001* _ _ Non-sinus rhythm 1.817 (0.601–5.498) 0.290 _ _ IHD 1.431 (0.517–3.956) 0.490 _ _ HHD 0.335 (0.184–0.609) < 0.001* _ _ CI, confidence interval; HHD, hypertensive heart disease; HR, heart rate; IHD, ischaemic heart disease; LVEF, left ventricular ejection fraction; MV E/A, transmitral early to late ventricular filling velocity ratio; NYHA, New York Heart Association; OR, odds ratio; PASP, pulmonary artery systolic pressure; SBP, systolic blood pressure. aNagelkerke R2 = 0.424, p < 0.001. *p-value is statistically significant.
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