Daily Cardiology Research Analysis
Across cardiology, three studies stand out: an individual patient data meta-analysis shows that the percentage of time ambulatory blood pressure stays within ESC 2024 targets (PTTR) robustly predicts mortality and cardiovascular events and outperforms office blood pressure. A 70,367-patient CCTA cohort links even moderate chronic kidney disease to significantly higher MACE rates, including among those with non-obstructive CAD. A countywide post-mortem study reveals that hypertrophic cardiomyopat
Summary
Across cardiology, three studies stand out: an individual patient data meta-analysis shows that the percentage of time ambulatory blood pressure stays within ESC 2024 targets (PTTR) robustly predicts mortality and cardiovascular events and outperforms office blood pressure. A 70,367-patient CCTA cohort links even moderate chronic kidney disease to significantly higher MACE rates, including among those with non-obstructive CAD. A countywide post-mortem study reveals that hypertrophic cardiomyopathy is an underdiagnosed contributor to sudden arrhythmic death, especially in people under 35.
Research Themes
- Ambulatory blood pressure time-in-target and outcomes
- CKD-CAD interaction on CCTA and cardiovascular risk
- Hidden burden of hypertrophic cardiomyopathy in sudden death
Selected Articles
1. Ambulatory blood pressure monitoring, European guideline targets, and cardiovascular outcomes: an individual patient data meta-analysis.
Across 14 cohorts (n=14,230; median follow-up 10.9 years), more time that ambulatory BP remains within ESC 2024 targets (PTTR) was strongly associated with lower mortality and cardiovascular events, independent of covariates. PTTR outperformed office BP at classifying BP control and the ESC 2024 thresholds shortened the time required to achieve meaningful risk reduction.
Impact: Introduces PTTR as a practical, quantitative BP control metric with strong prognostic discrimination, likely to influence guideline adoption of ABPM-derived targets and clinical workflows.
Clinical Implications: Incorporate ABPM-derived PTTR into routine risk assessment and treatment titration; prioritize achieving longer time-in-target rather than single office readings; consider ESC 2024 thresholds to accelerate risk reduction.
Key Findings
- Each increase in 24-h PTTR was associated with substantially lower all-cause mortality (HR 0.57) and cardiovascular endpoints (HR 0.30).
- Daytime/nighttime PTTR and cause-specific outcomes (CV mortality, coronary events, stroke) confirmed the association across subgroups.
- ESC 2024 targets reduced the time needed to achieve a 60% relative risk reduction from 14.4 to 4.3 hours compared with 2018 definitions; office BP misclassified most individuals versus PTTR.
Methodological Strengths
- Individual patient data meta-analysis across 14 cohorts with standardized PTTR definitions
- Long median follow-up (10.9 years) with robust multivariable adjustment and subgroup confirmations
Limitations
- Observational cohorts may retain residual confounding despite adjustment
- Heterogeneity in ABPM protocols and devices across cohorts cannot be fully excluded
Future Directions: Prospective interventional trials targeting PTTR, integration into digital hypertension management, and validation in high-risk and underrepresented populations.
2. Countywide burden, pathology, and genetics of lethal hypertrophic cardiomyopathy: from the POST SCD study.
In an 11-year countywide post-mortem cohort (n=1,022 presumed SCDs), HCM accounted for 2% of autopsy-confirmed arrhythmic deaths, with the greatest burden in individuals <35 years. Notably, 85% of HCM-related deaths were undiagnosed ante-mortem, indicating substantial under-recognition.
Impact: Provides rare, population-level, autopsy-anchored quantification of HCM’s contribution to sudden death and highlights a large diagnostic gap, particularly in the young.
Clinical Implications: Support enhanced screening and family-based evaluation in suspected HCM, consider athletic/young populations for targeted detection strategies, and integrate genetic testing pathways after sudden death.
Key Findings
- HCM represented 2% of autopsy-confirmed arrhythmic deaths across ages and 9.4% among arrhythmic deaths in those <35 years.
- Only 15% (2/13) of HCM-related presumed SCD cases had a pre-mortem diagnosis; 85% were undiagnosed.
- Genetic testing in consented pSCDs identified pathogenic/likely pathogenic variants in a substantial proportion and detected an additional case without clinical phenotype.
Methodological Strengths
- Prospective, countywide, post-mortem cohort with adjudicated arrhythmic vs non-arrhythmic causes
- Triangulation using pathology, TTE re-review, and genetic criteria
Limitations
- Small absolute number of HCM cases limits precision of subgroup estimates
- Genetic testing was not universal and may be influenced by consent and tissue availability
Future Directions: Evaluate community screening strategies in youth and athletes, refine post-mortem genetic workflows, and develop risk tools to identify silent HCM prior to catastrophic events.
3. Prognostic impact of reduced kidney function in patients with suspected coronary artery disease undergoing CCTA.
Among 70,367 symptomatic patients undergoing CCTA, reduced eGFR independently predicted higher MACE rates across CAD severities, including non-obstructive CAD. Notably, patients with non-obstructive CAD and eGFR 30–59 had event rates similar to those with potentially obstructive stenosis but higher eGFR, and guideline-directed lipid therapy was underused.
Impact: Defines CKD as a strong risk amplifier in CCTA-defined CAD, including non-obstructive disease, with immediate implications for preventive therapy gaps.
Clinical Implications: Aggressively risk-stratify CCTA patients with eGFR <60; intensify preventive therapies (lipid-lowering, BP control, SGLT2i/GLP-1RA where appropriate) even with non-obstructive CAD; close follow-up for ischemic events.
Key Findings
- Compared to eGFR ≥90, MACE risk increased with eGFR 60–89 (HR 1.09) and 30–59 (HR 1.42) after CCTA.
- In non-obstructive CAD, eGFR 30–59 had MACE rates similar to patients with potentially obstructive stenosis and higher eGFR.
- Guideline-recommended lipid-lowering therapy was underutilized in patients with reduced kidney function prior to CCTA.
Methodological Strengths
- Very large consecutive cohort (n=70,367) with standardized CCTA-based CAD stratification
- Event-driven analysis with clinically meaningful endpoints and multivariable adjustment
Limitations
- Observational design with potential residual confounding
- Renal function assessed at a single timepoint; albuminuria and longitudinal eGFR decline not incorporated
Future Directions: Prospective trials testing intensified prevention in non-obstructive CAD with CKD, and integration of kidney biomarkers (albuminuria, cystatin C) into CCTA risk models.