Cocaine and/or marijuana use is present in 10% of patients with an MI at age ≤50 years and is associated with worse all-cause and cardiovascular mortality. These findings reinforce current recommendations for substance use screening among young adults with an MI, and they highlight the need for counseling to prevent future adverse events.
Background:
Racial inequities for patients with heart failure (HF) have been widely documented. HF patients who receive cardiology care during a hospital admission have better outcomes. It is unknown whether there are differences in admission to a cardiology or general medicine service by race. This study examined the relationship between race and admission service, and its effect on 30-day readmission and mortality
Methods:
We performed a retrospective cohort study from September 2008 to November 2017 at a single large urban academic referral center of all patients self-referred to the emergency department and admitted to either the cardiology or general medicine service with a principal diagnosis of HF, who self-identified as white, black, or Latinx. We used multivariable generalized estimating equation models to assess the relationship between race and admission to the cardiology service. We used Cox regression to assess the association between race, admission service, and 30-day readmission and mortality.
Results:
Among 1967 unique patients (66.7% white, 23.6% black, and 9.7% Latinx), black and Latinx patients had lower rates of admission to the cardiology service than white patients (adjusted rate ratio, 0.91; 95% CI, 0.84–0.98, for black; adjusted rate ratio, 0.83; 95% CI, 0.72–0.97 for Latinx). Female sex and age >75 years were also independently associated with lower rates of admission to the cardiology service. Admission to the cardiology service was independently associated with decreased readmission within 30 days, independent of race.
Conclusions:
Black and Latinx patients were less likely to be admitted to cardiology for HF care. This inequity may, in part, drive racial inequities in HF outcomes.
Background
Calmodulin (CaM) mutations are associated with cardiac arrhythmia
susceptibility including the congenital long QT syndrome (LQTS).
Objective
To determine the clinical, genetic and functional features of two
novel CaM mutations in children with life-threatening ventricular
arrhythmias.
Methods
The clinical and genetic features of two congenital arrhythmia cases
associated with two novel calmodulin gene mutations were ascertained.
Biochemical and functional investigations were done on the two
mutations.
Results
A novel, de novo CALM2 mutation (D132H) was
discovered by candidate gene screening in a male infant with prenatal
bradycardia born to healthy parents. Postnatal course was complicated by
profound bradycardia, prolonged QTc (651 msec), 2:1 atrioventricular block
and cardiogenic shock. He was resuscitated and was treated with a cardiac
device. A second novel, de novo mutation in
CALM1 (D132V) was discovered by clinical exome
sequencing in a three year-old boy who suffered witnessed cardiac arrest
secondary to ventricular fibrillation. ECG recording after successful
resuscitation revealed a prolonged QTc of 574 msec. The
Ca2+ affinity of CaM-D132H and CaM-D132V revealed
extremely weak binding to the C-domain with significant structural
perturbations noted for D132H. Voltage-clamp recordings of human induced
pluripotent stem cell (iPSC) derived cardiomyocytes transiently expressing
wildtype or mutant CaM demonstrated that both mutations caused impaired
Ca2+-dependent inactivation (CDI) of voltage-gated
Ca2+ current. Neither mutant affected
voltage-dependent inactivation.
Conclusion
Our findings implicate impaired CDI in human cardiomyocytes as the
plausible mechanism for LQTS associated with two novel CaM mutations. The
data further expand the spectrum of genotype and phenotype associated with
calmodulinopathy.
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