\documentclass[10pt]{article}

\usepackage{fullpage}
\usepackage{setspace}
\usepackage{parskip}
\usepackage{titlesec}
\usepackage[section]{placeins}
\usepackage{xcolor}
\usepackage{breakcites}
\usepackage{lineno}
\usepackage{hyphenat}





\PassOptionsToPackage{hyphens}{url}
\usepackage[colorlinks = true,
            linkcolor = blue,
            urlcolor  = blue,
            citecolor = blue,
            anchorcolor = blue]{hyperref}
\usepackage{etoolbox}
\makeatletter
\patchcmd\@combinedblfloats{\box\@outputbox}{\unvbox\@outputbox}{}{%
  \errmessage{\noexpand\@combinedblfloats could not be patched}%
}%
\makeatother


\usepackage{natbib}




\renewenvironment{abstract}
  {{\bfseries\noindent{\abstractname}\par\nobreak}\footnotesize}
  {\bigskip}

\titlespacing{\section}{0pt}{*3}{*1}
\titlespacing{\subsection}{0pt}{*2}{*0.5}
\titlespacing{\subsubsection}{0pt}{*1.5}{0pt}


\usepackage{authblk}


\usepackage{graphicx}
\usepackage[space]{grffile}
\usepackage{latexsym}
\usepackage{textcomp}
\usepackage{longtable}
\usepackage{tabulary}
\usepackage{booktabs,array,multirow}
\usepackage{amsfonts,amsmath,amssymb}
\providecommand\citet{\cite}
\providecommand\citep{\cite}
\providecommand\citealt{\cite}
% You can conditionalize code for latexml or normal latex using this.
\newif\iflatexml\latexmlfalse
\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}}%

\AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}}

\usepackage[utf8]{inputenc}
\usepackage[english]{babel}



\usepackage{float}








\begin{document}

\title{Stress Kills}



\author[1]{Berhane Worku}%
\author[2]{shudhansu alishetti}%
\author[3]{kumudha ramasubba}%
\affil[1]{New York Presbyterian Weill Cornell Medicine}%
\affil[2]{NewYork-Presbyterian Brooklyn Methodist Hospital}%
\affil[3]{Affiliation not available}%


\vspace{-1em}



  
  \date{May 23, 2024}


\begingroup
\let\center\flushleft
\let\endcenter\endflushleft
\maketitle
\endgroup








\sloppy


Stress Kills

Berhane Worku MD\textsuperscript{1}, Shudhanshu
Alishetti\textsuperscript{2}, Kumudha Ramasubbu\textsuperscript{2}

1. New York Presbyterian Brooklyn Methodist Hospital/Weill Cornell
Medical Center Department of Cardiothoracic Surgery, Brooklyn, NY 11215

2. New York Presbyterian Brooklyn Methodist Hospital Division of
Cardiology, Brooklyn NY 11215

Corresponding Author

Berhane Worku MD

Department of Cardiothoracic Surgery

New York Presbyterian Brooklyn Methodist Hospital

506 6\textsuperscript{th} Street

Brooklyn, NY 11215

The medical, economic, and social consequences of the COVID-19 pandemic
have been profound. Severe respiratory failure as well as inflammatory
and thrombotic complications have resulted in hundreds of thousands of
deaths. Political controversy continues regarding optimal strategies for
large scale control of the pandemic. Social distancing policies have led
to reduced transmission rates but the economic effects have been
devastating. Optimal treatment strategies continue to evolve, and
vaccine solutions are on the horizon. In addition to these more obvious
issues, other severe consequences of the pandemic are slowly being
recognized.

In the current report, Kir et. al. describe two postmenopausal women
presenting with signs and symptoms of acute coronary syndrome in the
setting of severe psychological stress related to social isolation
during the COVID-19 pandemic (1). Both were COVID negative and both had
unremarkable coronary angiograms. Both were diagnosed with takotsubo
cardiomyopathy based on the characteristic findings of angina, mild
troponin elevation, electrocardiographic changes, and apical akinesis on
echocardiogram. Both admitted to severe anxiety and stress in the days
prior to the onset of symptoms. Both improved with conservative
management including beta-blockers and anxiolytics with resolution of
apical akinesis on follow up echocardiogram.

Takotsubo or stress cardiomyopathy is a now well recognized entity
typically presenting as angina or dyspnea in the setting of a severe
emotional or physical stressor. Postmenopausal women are more frequently
affected and a history of psychiatric disorders is frequently noted.
Electrocardiographic abnormalities and mild troponin elevations are
common. Diagnosis is based on the InterTAK diagnostic score.
Echocardiography classically demonstrates apical ballooning with basal
hyperkinesis, but other wall motion abnormalities are described usually
extending beyond a traditional coronary artery distribution. Coronary
angiography is frequently performed to rule out acute coronary syndrome
but is unremarkable. The syndrome is typically self-limited, requiring
conservative supportive management, but in severe cases can lead to
heart failure and shock requiring high-dose pharmacologic support,
mechanical circulatory support, and in \textasciitilde{}5\% of cases can
be fatal (2).

Emotional and physical stress are risk factors for a variety of
conditions including cardiovascular disease. Furthermore, psychiatric
disorders such as depression and anxiety are associated with poorer
outcomes in the setting of cardiovascular disease. Proposed mechanisms
for this include behavioral factors such as noncompliance with
medications and lifestyle modifications (diet, exercise, smoking
cessation). Biological factors are also suggested, including altered
autonomic nervous system activity with elevations in catecholamine
levels and inflammatory responses amongst others (3). Similar hypotheses
have been put forth regarding the mechanism of takotsubo stress
cardiomyopathy and perhaps some overlap exists between the
cardiovascular manifestations of psychiatric disorders and overt stress
cardiomyopathy.

The COVID-19 pandemic has had several medical consequences beyond those
related to viral infection itself. The suspension of certain medical and
surgical services potentially allows for the natural history of various
diseases to take their course. Unemployment impairs the ability of many
to access what medical services remain available. Psychiatric disorders
are inflamed in the setting of social, economic, and other stressors. A
four to five-fold increase in the incidence of stress cardiomyopathy has
been noted during the months following the COVID-19 outbreak unrelated
to COVID-19 infection itself, presumably the consequence of stress
related to the abovementioned effects of the pandemic and our response
to it. (4). COVID-19 has taught us that stress kills.

REFERENCES

\begin{enumerate}
\tightlist
\item
  Kir D, Beer N, De Marchena EJ. Takutsobo cardiomyopathy caused by
  emotional stressors in the Coronavirus Disease 2019 (COVID-19)
  pandemic era. J Card Surg in press
\item
  De Chazal HM, Del Buono MG, Keyser-Marcus L, Ma L, Moeller FG,
  Berrocal D, Abbate A. Stress cardiomyopathy diagnosis and treatment. J
  Am Coll Cardiol 2018;72:1955-71
\item
  Takagi H, Ando T, Umemoto. Perioperative depression or anxiety and
  postoperative mortality in cardiac surgery: a systematic review and
  meta-analysis. Heart Vessels 2017;32:1458-1468
\item
  Jabri A, Kalra a, Kumar A, Alameh A, Adroja S, Bashir H, Nowacki AS,
  Shah R, Khubber S, Kanaa'N A, Hedrick DP, Sleik KM, Mehta N, Chung MK,
  Khot UN, Kapadia SR, Puri R, Reed GW. Incidence of stress
  cardiomyopathy during the coronavirus disease 2019 pandemic. JAMA Netw
  Open 2020 Jul 1;3(7):e2014780.~doi: 10.1001/jamanetworkopen.2020.14780
\end{enumerate}

\selectlanguage{english}
\FloatBarrier
\end{document}

