Key result
Resting hypercontractile phenotype linked to ~53% higher all-cause mortality versus normal elastance in CCS.
Why the study?
To evaluate the prognostic significance and functional correlates of a hypercontractile phenotype identified by resting transthoracic echocardiography in chronic coronary syndromes.
Does a hypercontractile phenotype at rest predict increased mortality and impaired functional reserve in patients with chronic coronary syndromes?
Cohort (n=10,677)
Yes
Does a hypercontractile phenotype at rest predict increased mortality and impaired functional reserve in patients with chronic coronary syndromes?
A hypercontractile phenotype at rest in chronic coronary syndromes is paradoxically associated with impaired functional reserve and increased all-cause mortality.
Answers are grounded in this paper and cite their sources.
Hypercontractile phenotype may flag higher mortality risk in CCS; hypothesis-generating and should not yet change practice.
BACKGROUND: Transthoracic echocardiography (TTE) identifies a hypercontractile phenotype (HP) in chronic coronary syndromes (CCS), characterized by elevated resting left ventricular (LV) elastance (Force = systolic blood pressure/end-systolic volume). OBJECTIVES: To evaluate the prognostic significance and functional correlates of HP. METHODS: In a prospective multicenter study, 10,677 CCS patients underwent resting TTE to assess LV ejection fraction (EF), stroke volume (SV), and force by quantitative volumetric echocardiography. All patients were followed for the endpoint of all-cause mortality. In a subset of 5,834 patients, stress echocardiography (exercise or dobutamine) was performed for LV contractile reserve (LVCR) and heart rate reserve (HRR). RESULTS: Patients were stratified into Force quintiles (Q1-Q5). HP patients exhibited lower SV at rest (Q5=34.8±12.3 vs. Q1-Q4=57.4 ± 19.1 mL; p<0.01) and higher EF at rest (Q5=64.8±6.9% vs. Q1-Q4= 58.1±8.7%, p<0.01). During a median follow-up of 24 months (interquartile range=12- 40 months), 509 deaths occurred. The exposure-adjusted death rate was lowest in Q3 (3.53-4.51 mmHg/mL; 1.03 per 100 person/years) and higher in Q1 (≤2.62 mmHg/mL, 2.88), Q2 (2.63-3.52 mmHg/mL, 1.86), Q4 (4.52-6.11 mmHg/mL,1.56), and Q5 (HP, >6.11 mmHg/mL; 1.88; p<0.0001 vs. Q1 and Q3). Multivariable analysis identified HP (Q5; HR 1.531 vs Q3, 95% CI 1.116-2.099; p=0.006) and EF (HR 0.963, 95% CI 0.953-0.972; p<0.0001) as independent predictors of death. During exercise or dobutamine stress, HP showed reduced LVCR (ΔEF: Q5 = 4.3± 9.4% vs. Q1-Q4 = 7.0±9.3%; p<0.001) and blunted HRR (Q5 = 1.77± 0.33 vs. Q1-Q4 = 1.85±0.39; p<0.01). All patients with force-based LV contractile reserve >4.1 (present in 185, 3.2% of the population) survived. CONCLUSIONS: CCS patients with HP assessed by resting TTE demonstrate higher mortality and multilayered functional impairment, including reduced LV contractile and chronotropic reserves. HP improved the prediction of mortality by EF. A "stronger" heart is, in fact, functionally and prognostically weaker.
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Ciampi et al. (2026) conducted a cohort in Chronic coronary syndromes (n=10,677). Hypercontractile phenotype (Force >6.11 mmHg/mL) vs. Normal resting elastance (Force quintile 3: 3.53-4.51 mmHg/mL) was evaluated on All-cause mortality (HR 1.531, 95% CI 1.116-2.099, p=0.006). In patients with chronic coronary syndromes, a resting hypercontractile phenotype was associated with increased all-cause mortality compared to normal elastance (HR 1.531; 95% CI 1.116-2.099; p=0.006).
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