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.
BACKGROUND AND AIMS: Hypertension is the predominant modifiable cardiovascular risk factor. This cohort study assessed the association of risk with the percentage of time that the ambulatory blood pressure (ABP) is within the target range (PTTR) proposed by the 2024 European Society of Cardiology (ESC) guidelines for blood pressure (BP) management. METHODS: In a person-level meta-analysis of 14 230 individuals enrolled in 14 population cohorts, systolic and diastolic ABPs were combined to assess 24-h, daytime, and nighttime PTTR with thresholds for non-elevated ABP set at <115/65, <120/70, and <110/60 mmHg, respectively. RESULTS: Median 24-h PTTR was 18% (interquartile range 5-33) corresponding to 4.3 h (1.2-7.9). Over 10.9 years (median), deaths (N = 3117) and cardiovascular endpoints (N = 2265) decreased across increasing 24-h PTTR quartiles from 21.3 to 16.1 and from 20.3 to 11.3 events per 1000 person-years. The standardized multivariable-adjusted hazard ratios for 24-h PTTR were 0.57 (95% confidence interval 0.46-0.71) for mortality and 0.30 (0.23-0.39) for cardiovascular endpoints. Analyses of daytime and nighttime ABP, cardiovascular mortality, coronary endpoints and stroke, and subgroups produced confirmatory results. The 2024 ESC non-elevated 24-h PTTR, compared with the 2018 ESC/European Society of Hypertension non-hypertensive 24-h PTTR, shortened the interval required to reduce relative risk for adverse outcomes from 60% to 18% (14.4-4.3 h). Office BP, compared with 24-h PTTR, misclassified most participants with regard to BP control. CONCLUSIONS: Longer time that ABP is within the 2024 ESC target range is associated with reduced adverse outcomes; PTTR derived from ABP refines risk prediction and compared with office BP avoids misclassification of individuals with regard to BP control.
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.
AIMS: Incidence of sudden cardiac death (SCD) is 1%/year in cohorts with hypertrophic cardiomyopathy (HCM), but this estimate presumes arrhythmic cause and misses occult cases dying before diagnosis. METHODS AND RESULTS: POST SCD (POstmortem Systematic InvesTigation of Sudden Cardiac Death) is a prospective cohort study using autopsy, clinical records, and toxicology to adjudicate arrhythmic or non-arrhythmic causes among presumed SCDs (pSCDs) meeting WHO criteria aged 0-90 years in San Francisco County. We included all incident cases 2/1/2011-3/1/2014 (n = 525) and approximately every third day 3/1/2014-9/1/2022 (n = 497) based on medical examiner call schedule. We identified HCM victims via three approaches: (i) pathology; (ii) echocardiogram [transthoracic echocardiogram (TTE)]; (iii) genetic criteria. Incidence calculations used county data and estimated HCM prevalence of 1:500 from studies of persons aged 23-35 years old. Of 1022 pSCDs [558 (54.6%) arrhythmic deaths] during the study period, 13 had HCM: 10 met pathology criteria; 2 via review of 203 TTEs (missed on initial report); 1 via genetic testing. Of these, 11 were arrhythmic deaths, yielding 1.3% burden of sudden death (pSCD) and 2% of arrhythmic death. Only 2 of 13 (15%) pSCDs with HCM had pre-mortem diagnosis. Incidence for persons with HCM 18-35 years old was 0.2% pSCDs/year and 0.1% SADs/year. pSCDs with HCM had a higher proportion of arrhythmic cause [11/13 (85%) vs. 547/1009 (54%), P = 0.03] than those without. pSCD burden due to HCM decreased with age (P = 0.003), highest among victims <35 years old, for whom HCM accounted for 7.1% of pSCD and 9.4% of arrhythmic death. Genetic testing of 317 consented pSCDs yielded pathogenic or likely pathogenic variants in 40% (2/5) and identified one additional case without clinical phenotype. CONCLUSION: In this 11-year countywide post-mortem study, HCM meeting pathologic, clinical, or genetic criteria was associated with autopsy-confirmed arrhythmic cause of sudden death, accounting for 2% of SADs up to age 90, highest in cases <35 years old. Since 85% of cases were undiagnosed before pSCD, the true burden of HCM-related sudden death may be substantially underestimated.
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.
AIMS: Chronic kidney disease (CKD) and coronary artery disease (CAD) share common risk factors, but the association between kidney function (estimated glomerular filtration rate (eGFR) in mL/min/1.73 m²) and major adverse cardiovascular events (MACE) in patients undergoing coronary computed tomography angiography (CCTA) due to suspected CAD has not been established. This study investigated the association between kidney function and MACE in symptomatic patients undergoing CCTA. METHODS: A cohort study of consecutive, symptomatic patients undergoing CCTA between 2008 and 2021 (N=70,367). CAD severity was stratified as no CAD, non-obstructive CAD, and obstructive CAD (≥50% diameter stenosis). The primary outcome was MACE (myocardial infarction, ischemic stroke, or cardiovascular death). eGFR was calculated based on plasma creatinine at the time of CCTA. RESULTS: In total, 41,156 (59%) had eGFR ≥90, 27,011 (38%) had eGFR 60-89, and 2200 (3%) had eGFR 30-59. Median follow-up were 5.1 years, according to eGFR ≥90, 60-89, and 30-59 groups, MACE rates per 1000 person-years in patients with obstructive CAD were 14.2, 15.4, and 25.8, respectively and in patients with non-obstructive CAD the MACE rates were 6.4, 8.0, and 14.4, respectively. Compared to patients with eGFR ≥90, hazard ratios for MACE were 1.09 (95% confidence intervals (CI) 1.00-1.19) and 1.42 (95%CI 1.18-1.69) for patients with eGFR 60-89 and 30-59, respectively. CONCLUSION: In patients referred for CCTA due to suspected CAD, reduced kidney function was associated with an increased rate of MACE. Therefore, CKD is a strong independent cardiovascular risk factor, particularly in patients with CAD detected on CCTA. In individuals with evidence of coronary artery disease a reduced kidney function significantly increases the risk of ischemic events and death.Patients with non-obstructive coronary artery disease and eGFR 30-59 have similar incidence rates of major adverse events and deaths as patients with eGFR > 60 and potentially obstructive stenosis on coronary CT angiography.Only a minority of patients with reduced kidney function receive guideline recommended lipid-lowering therapy prior to coronary CT angiography, and optimization of cardiovascular preventive therapy in patients with reduced kidney function is warranted.