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Table of Contents
CASE REPORT
Year : 2022  |  Volume : 19  |  Issue : 3  |  Page : 187-189

Sepsis-induced suicidal left ventricular in a patient with hypertrophic cardiomyopathy/hypertrophic obstructive cardiomyopathy


1 Department of Cardiology, Apollo Hospital, Indore, Madhya Pradesh, India
2 Department of Cardiology and Critical Care, Apollo Hospital, Indore, Madhya Pradesh, India

Date of Submission22-Apr-2022
Date of Decision25-Jun-2022
Date of Acceptance27-Jun-2022
Date of Web Publication05-Aug-2022

Correspondence Address:
K Roshan Rao
Department of Cardiology, Apollo Hospital, Indore, Madhya Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/am.am_66_22

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  Abstract 


Hypertrophic cardiomyopathy is the most common heritable cardiomyopathy, manifesting as left ventricular hypertrophy. In this case, a 48-year-male patient presented with complaints of shortness of breath, uneasiness for 15 days, right lower limb pain, and one episode of fever for 2 days. He was initiated on antibiotics but gradually started developing hypotension and oliguria. After optimizing the medical therapy and as a life-saving measure, alcoholic septal ablation was done in this patient as a last resort. The patient was weaned off the ventilator after 72 h and discharged in a stable condition. He has continued follow-up for 8 months and is asymptomatic; the gradient has not recurred. The patient had both issues, and timely alcohol septal ablation helped save the patient by optimizing the hemodynamics. This is a rare situation of suicidal left ventricular induced by sepsis-induced vasodilation.

Keywords: HCM, HOCM, LVOT


How to cite this article:
Rao K R, Rao S, Gupta A. Sepsis-induced suicidal left ventricular in a patient with hypertrophic cardiomyopathy/hypertrophic obstructive cardiomyopathy. Apollo Med 2022;19:187-9

How to cite this URL:
Rao K R, Rao S, Gupta A. Sepsis-induced suicidal left ventricular in a patient with hypertrophic cardiomyopathy/hypertrophic obstructive cardiomyopathy. Apollo Med [serial online] 2022 [cited 2022 Sep 30];19:187-9. Available from: https://apollomedicine.org/text.asp?2022/19/3/187/353351




  Introduction Top


Hypertrophic cardiomyopathy (HCM) is the most common autosomal dominant form of the inherited primary myocardial disorder, characterized by hypertrophy or thickening of the left (sometimes right) ventricles with histological features of myocyte hypertrophy, myofibrillar disarray, and interstitial fibrosis.[1] It affects one case per 200–500 persons and often remains clinically silent.[2]

Patient presentation varies from asymptomatic to heart failure (HF) or sudden cardiac death (SCD). In most patients, the left ventricular hypertrophy (LVH) and abnormal ventricular configuration cause dynamic left ventricular (LV) outflow blockage. Therapeutic approaches primarily aim to minimize emotional blockage, with treatment options including lifestyle changes, pharmacotherapies, and septal reduction techniques.[3] Septal ablation is technically tricky in hemodynamically unstable patients. The patient started to improve after alcohol septal ablation. It is a challenge for the operator also.


  Case Report Top


We report here a case of a 48-year-male, known Hypertension (HTN) and chronic ethanol drinker, who presented with complaints of shortness of breath, uneasiness for 15 days, right lower limb pain, and fever for 2 days.

On evaluation, the right lower limb had no evidence of thrombosis but s/o cellulitis. His electrocardiogram had an LVH pattern, and his echocardiography showed normal LVF and hypertrophic obstructive cardiomyopathy with an left ventricular outflow tract (LVOT) gradient of 177 mmHg [Figure 1]. His coronary angiography was routine. He was initiated on antibiotics but gradually started developing hypotension and oliguria.
Figure 1: Preprocedure LVOT gradient. LVOT: Left ventricular outflow tract

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The arterial line was cannulated, which showed a blood pressure (BP) of 70/40 mmHg. As sepsis is a vasodilatory state and requires fluids as per sepsis protocol, he was given fluids, but because of the high LVOT gradient, the patient landed in acute LVF. He was managed initially with noninvasive ventilation support, but as he was unable to maintain saturations that were taken on invasive mechanical ventilation. He worsened over hours because of sepsis-induced vasodilator and worsening LVOT gradient, and falling BP despite phenylephrine (1.25 mcg/kg/min), noradrenaline (2.5 mcg/kg/min), vasopressin (1.2 ml per h 0.03units per min), and fluids. Hence, as a life-saving measure, alcoholic septal ablation was done in this patient as a last resort. The patient hemodynamic condition started improving and his urine output improved. His LVOT gradient decreased to 50 [Figure 2]. The patient was weaned off the ventilator after 72 h and discharged in a stable condition. He is in continued follow-up for 8 months, asymptomatic, and the gradient has not recurred.
Figure 2: Postprocedure LVOT gradient. LVOT: Left ventricular outflow tract

Click here to view



  Discussion and Conclusion Top


HCM is a genetically determined cardiac muscle disease caused most commonly (60%–70%) by mutations in one of many sarcomere genes that encode components of the heart's contractile mechanism.

Men are more likely affected than women by HCM.[4] Wang et al.[5] found that women under 50 have a worse prognosis than those over 50. HCM patients live near-normal lives, with a survival rate of around 96%, unless they die suddenly due to exertion or arrhythmia.[6]

According to one study, patients with symptomatic nonobstructive HCM have a latent LVOT obstruction that does not manifest until the LV function is stressed.

LVH of diverse morphologies characterizes HCM, which has a wide range of clinical symptoms and hemodynamic problems. Patients with HCM may develop one or more of the following anomalies, depending on the site and extent of heart hypertrophy:

  • Obstruction of the LV outflow
  • Diastolic dysfunction
  • Myocardial ischemia
  • Regurgitation of the mitral valve.


A range of symptoms can result from these structural and functional problems, including:

  • Chest pain
  • Dyspnea
  • Fatigue
  • Palpitations
  • Syncope or Presyncope.


HF, chest discomfort, and arrhythmias are the three primary symptoms associated with HCM. Patients with HCM are more likely to develop supraventricular and ventricular arrhythmias and a higher risk of SCD.

HF, most commonly manifesting as dyspnea on exertion, is the most common presentation in persons with HCM, occurring in over 90% of symptomatic patients. Dyspnea can result from a variety of mechanisms:

  • Diastolic dysfunction due to myocardial hypertrophy
  • Impaired LV emptying due to LVOT obstruction, resulting in increased LV end-diastolic pressure
  • Mitral regurgitation (MR)
  • Systolic dysfunction in a patient with more extensive myocardial involvement.


The hemodynamics are very peculiar in that any pathological or physiological maneuver which decreases LV size by reducing afterload or preload results in aggravation of the dynamic obstruction and causing a variety of new or sudden onset symptoms.

Now, in septic shock, a vasodilatory condition, intravascular hypovolemia is typical and may be severe, thus acting in both ways by reducing preload and after load requiring rapid fluid resuscitation and vasoconstriction.

Intravascular hypovolemia is common in sepsis and can be dangerous. Unless there is strong evidence of considerable pulmonary edema, rapid, and large-volume IVF infusions (30 mL/kg) are recommended as first-line therapy for severe sepsis or septic shock. Which was there in our patient and was due to suicidal LV, or a separate physiological entity which has a normal systolic function but more of mid systolic MR.

Hence, managing both the conditions in the same patient is challenging.

Our patient also had both the issues, timely alcohol septal ablation helped to save the patient by optimizing the hemodynamics, and this is a rare situation of suicidal LV induced by sepsis-induced vasodilation, not reported in the literature, to the best of our knowledge as an entity sepsis-induced vasodilation, leading suicidal LV.

Informed consent

Informed consent was obtained from the patient.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Acknowledgment

The author would like to thank the patient for his kind permission to publish this case report.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Author Contribution

Dr K. Roshan Rao: Conception of the idea, Drafting the article, Critical revision of the article, and final approval of the version to be published. Dr Sarita Rao: Drafting the article, Critical revision of the article, and final approval of the version to be published. Dr Ankur Gupta: Critical revision of the article.



 
  References Top

1.
Biswas A, Das S, Kapoor M, Seth S, Bhargava B, Rao VR. Epidemiology of cardiomyopathy – The EPOCH-H study is a clinical and genetic study of hypertrophic cardiomyopathy. J Pract Cardiovasc Sci 2015;1:143-9.  Back to cited text no. 1
  [Full text]  
2.
Maron BJ. Clinical course and management of hypertrophic cardiomyopathy. N Engl J Med 2018;379:655-68.  Back to cited text no. 2
    
3.
Geske JB, Ommen SR, Gersh BJ. Hypertrophic cardiomyopathy: Clinical update. JACC Heart Fail 2018;6:364-75.  Back to cited text no. 3
    
4.
Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, et al. 2011 ACCF/AHA guideline for diagnosing and treating hypertrophic cardiomyopathy. J Am Coll Cardiol 2001;142:e153-203.  Back to cited text no. 4
    
5.
Wang Y, Wang J, Zou Y, Bao J, Sun K, Zhu L, et al. Female sex is associated with worse prognosis in patients with hypertrophic cardiomyopathy in China. PLoS One 2014;9:e102969.  Back to cited text no. 5
    
6.
Shah JS, Esteban MT, Thaman R, Sharma R, Mist B, Pantazis A, et al. Prevalence of exercise-induced left ventricular outflow tract obstruction in symptomatic patients with non-obstructive hypertrophic cardiomyopathy. Heart 2008;94:1288-94.  Back to cited text no. 6
    


    Figures

  [Figure 1], [Figure 2]



 

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