Colombo, Rosario

Introduction: Apolipoprotein B (ApoB) and coronary artery calcium score (CAC) are well-established risk factors for coronary heart disease (CHD). However, the interaction between these risk factors on CHD risk has not been well-studied. We investigated the association between ApoB levels and CAC with CHD risk. Methods: We analyzed 4,649 participants from the Multiethnic Study of Atherosclerosis cohort (median follow-up 13.9 years) without baseline CHD or statin use. High ApoB was defined as ≥120 mg/dL. Participants were divided into 6 groups; group 1: CAC = 0 with normal ApoB, group 2: CAC = 0 with high ApoB, group 3: CAC 1-99 with normal ApoB, group 4: CAC 1-99 with high ApoB, group 5: CAC ≥100 with normal ApoB, group 6: CAC ≥100 with high ApoB. CHD was defined as myocardial infarction, resuscitated cardiac arrest, or CHD death. Survival analysis using Kaplan-Meier and multivariable Cox proportional hazard models were performed to assess the relationship between ApoB, CAC, and time to first CHD event. Results: In an adjusted model, high ApoB, CAC (1-99), and CAC (≥100) were independently associated with CHD (HR: 1.48; 95% CI: 1.04, 2.11; HR: 2.54; 95% CI: 1.78, 3.64; and HR: 4.41; 95% CI: 3.08, 6.31, respectively). Compared to group 1 (CAC 0 with normal ApoB), CAC 0 and high ApoB (group 2) was not associated with increased risk of CHD (HR: 1.15; 95% CI: 0.59, 2.23). However, a statistically significant greater risk of CHD was observed in those with CAC 1-99 and normal ApoB (group 3) (HR: 2.12; 95% CI: 1.37, 3.28), CAC 1-99 and high ApoB (group 4) (HR: 4.12; 95% CI: 2.42, 7.00), CAC ≥100 and normal ApoB (group 5) (HR: 4.20; 95% CI: 2.78, 6.34), CAC ≥100 and high ApoB (group 6) (HR: 5.72; 95% CI: 3.40, 9.63). Conclusions: In this analysis, ApoB and CAC are independently associated with CHD risk. Individuals with high ApoB and CAC ≥100 had the highest risk of CHD. In contrast, individuals with CAC = 0 and high ApoB had no significant increase in CHD risk compared to individuals with normal ApoB levels. These findings suggest that ApoB and CAC may be complementary tools for CHD risk stratification in the context of primary prevention.

Background: Lipoprotein(a) [Lp(a)] and metabolic syndrome (MetS) are well-established risk factors for cardiovascular disease. Recent evidence suggests that high Lp(a) levels may increase the risk of coronary heart disease (CHD) in patients with diabetes, raising the question of whether similar interactions exist between Lp(a) and metabolic syndrome. We aimed to evaluate the joint association of Lp(a) and MetS with incident CHD risk in a large, multi-ethnic, prospective cohort. Methods: We analyzed 6,664 participants from the MESA (Multiethnic Study of Atherosclerosis) cohort (median follow-up 14.0 years) without baseline CHD. MetS was defined as ≥3 of the following criteria: waist circumference ≥102 cm (men), or ≥88 cm (women), triglycerides ≥150 mg/dL or use of a fibrate medication, HDL-C <40 (men) or <50 (women) or use of a fibrate medication, SBP ≥130 mm Hg and/or DBP ≥85 mm Hg or use of antihypertensive medication, fasting glucose ≥100 mg/dL or use of antidiabetic medication (4). Elevated Lp(a) was defined as a level ≥50 mg/dL. CHD was defined as myocardial infarction, resuscitated cardiac arrest, or CHD death. Participants were divided into four groups: group 1: Normal Lp(a) without MetS, group 2: elevated Lp(a) without MetS, group 3: normal Lp(a) with MetS, group 4: elevated Lp(a) with MetS. Survival analysis using Kaplan-Meier and multivariable Cox proportional hazard models were performed to assess the relationship between Lp(a), MetS, and time to CHD. Results: In an adjusted model, log [Lp(a)] and MetS were both independently associated with CHD (HR: 1.14; 95% CI: 1.03, 1.25) and (HR: 1.75; 95% CI: 1.35, 2.27). Compared to the reference group (normal Lp(a) without MetS), those with elevated Lp(a) without MetS (group 2) did not have increased risk of CHD (HR: 1.30; 95% CI: 0.94, 1.80). However, those with normal Lp(a) with MetS (group 3) had greater risk of CHD (HR: 1.56; 95% CI: 1.18, 2.05). The highest risk for CHD were in those with elevated Lp(a) with MetS (group 4) (HR: 2.37; 95% CI: 1.66, 3.37). Conclusions: In this analysis. elevated Lp(a) and MetS independently increase CHD risk. MetS alone significantly increases risk, whereas elevated Lp(a) without MetS does not demonstrate a significant effect. However, their combination confers the highest risk, suggesting a synergistic interaction. These results emphasize the value of assessing Lp(a) in individuals with MetS to improve cardiovascular risk stratification and guide targeted prevention.

Background: The comparable long-term benefits of coronary artery bypass grafting (CABG) versus percutaneous coronary intervention (PCI) in patients with multivessel disease remains limited in underrepresented populations, particularly in patients with multivessel coronary artery disease and heart failure with severely reduced left ventricular ejection fraction (LVEF <35%). Research Question: Among patients with HF and LVEF < 35% which revascularization strategy (CABG or PCI) provides superior long-term clinical outcomes? Methods: We conducted a systematic review and meta-analysis of observational studies involving patients with ischemic heart disease (IHD), HF and LVEF < 35% undergoing PCI or CABG with a minimum follow-up duration of five years. PubMed, Embase, and Cochrane databases were searched for studies published up to April 15, 2025. We computed hazard ratios (HR) from propensity score matched results. We used Cochrane Review Manager version 9.2.1 for statistical analysis. The primary endpoints of interest included all-cause mortality at 5 to 10 years, repeat revascularization, and all-cause mortality at 10 or more years. Results: We included 8 studies with 12,697 patients (6,187 PCI vs 6,510 CABG). Median follow-up duration ranged from 3.8 to 5.2 years, with the longest reported follow-up up to 13 years. The cumulative, propensity adjusted, incidence of all-cause mortality was significantly lower in the CABG group compared to PCI in 5 to 10 years of follow-up (HR 0.61; 95% CI 0.54-0.69; p<0.001) and ≥ 10 years (HR 0.63; 95% CI 0.53-0.74; p<0.001). Additionally, CABG was associated with a reduced need for repeat revascularization in the 5 to 10 year time frame, with a HR of 0.42 (95% CI 0.22-0.81; p=0.01). Conclusion: In this systematic review and meta-analysis of patients with IHD and an ejection fraction ≤ 35% undergoing revascularization, CABG was associated with a reduction in all-cause mortality at ≥ 5 and ≥ 10 years of follow-up, as compared to PCI.

Abstract Background Physical or emotional stress is the most common cause of Takotsubo cardiomyopathy (TS). The exact mechanism of TS remains unclear, and some possible mechanism include myocardial edema and inflammation, coronary vasospasm, microcirculatory dysfunction, catecholamine surge, and sympathetic overdrive. Recently, and consistent with the availability of coronary spasm provocative studies, data suggests that coronary artery vasospasm (CAVS) plays an essential role in the pathogenesis of TS. However, whether CAVS is a consequence or a primary cause of TS is still unclear. The clinical implications of concomitant TS and CAVS have not been studied. Purpose Describe differences in baseline characteristics, comorbidities, cardiovascular risk factors, in-hospital mortality, and outcomes of patients with TS and documented CAVS. Methods The US National Inpatient Database was queried from 2011 to 2019 for relevant ICD-9 and -10 diagnostic and procedural codes. We identified patients admitted with TS who had a coronary angiogram. We then excluded those who underwent coronary percutaneous coronary intervention (PCI), coronary artery bypass graft (CAGB) or had a diagnosis of myocarditis. We compared baseline characteristics and in-hospital outcomes of patients with TS with vs. without documented CAVS. Results We identified 136,732 patients admitted with TS, of which 1,112 (0.8%) had CAVS. We found that those patients with TS and CAVS were younger and less likely to have hypertension, diabetes, atrial fibrillation, hyperlipidemia, coronary artery disease, peripheral artery disease, chronic kidney disease, chronic obstructive pulmonary disease, a prior cancer diagnosis, and smoking history than those without CAVS. Conversely, they were more likely to be obese, have substance abuse disorder, a history of polycystic ovary syndrome, post-traumatic stress disorder, anxiety, history of migraines, and have had a prior myocardial infarction (MI). Regarding in-hospital outcomes, we did not find a significant difference in mortality between groups. Those with TS and CAVS were more likely to have a cardiac arrest, 2nd-degree AV block, ventricular fibrillation, ventricular tachycardia, and more likely to require ICD placement compared to those patients without CAVS. Conclusions Patients with TS and coronary vasospasm were younger, had fewer cardiovascular risk factors but were more likely to have had a prior MI than those without CAVS. We report no significant difference in mortality between groups. However, those with TS and CAVS were more likely to have hospitalizations complicated by cardiac arrest and significant arrhythmias like ventricular fibrillation, ventricular tachycardia, and 2nd-degree AV Block, which led to a higher need for ICD implantation. This large US nationwide retrospective study can provide hypotheses generating ideas for more extensive prospective studies to determine the frequency and role of CAVS in patients with TS.

Septal Myectomy (SM) and Alcohol Septal Ablation (ASA) improve symptoms in patients with Hypertrophic Cardiomyopathy with outflow tract obstruction (oHCM). However, outcomes data in this population is predominantly from specialized centers. The National Inpatient Database was queried from 2011 to 2019 for relevant international classification of diseases (ICD)-9 and -10 diagnostic and procedural codes. We compared baseline characteristics and in-hospital outcomes of patients with oHCM who underwent SM vs ASA. A p-value < 0.001 was considered statistically significant. We identified 15,119 patients with oHCM who underwent septal reduction therapies, of whom 57.4% underwent SM, and 42.6% underwent ASA. Patients who underwent SM had higher all-cause mortality (OR: 1.8 (1.3–2.5)), post-procedure ischemic stroke (OR: 2.3 (1.7–3.2)), acute kidney injury (OR: 1.4 (1.2–1.7)), vascular complications (OR: 3.6 (2.3–5.3)), ventricular septal defect (OR: 4.4 (3.2–6.1)), cardiogenic shock (OR: 1.7 (1.3–2.3)), sepsis (OR: 3.2 (1.9–5.4)), and left bundle branch block (OR: 3.5 (3–4)), compared to ASA. Patients who underwent ASA had higher post-procedure complete heart block (OR: 1.3 (1.1–1.4)), right bundle branch block (OR: 6.3 (5–7.7)), ventricular tachycardia (OR: 2.2 (1.9–2.6)), supraventricular tachycardia (OR: 1.6 (1.4–2)), and more commonly required pacemaker insertion (OR: 1.4 (1.3–1.7)) (p < 0.001 for all) compared to SM. This nationwide analysis evidenced that patients undergoing SM had higher in-hospital mortality and periprocedural complications than ASA; however, those undergoing ASA had more post-procedure conduction abnormalities and pacemaker implantation. The implications of these findings warrant further investigation regarding patient selection strategies for these therapies.