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 Table of Contents  
Year : 2017  |  Volume : 3  |  Issue : 3  |  Page : 163-165

A case of dilated cardiomyopathy

Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication1-Feb-2018

Correspondence Address:
Dr. Arvind Dambalkar
Department of Cardiology, All India Institute of Medical Sciences, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpcs.jpcs_58_17

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A case of heart failure (HF) presents for the first time. The management of HF from the first visit to the subsequent visits based on the current guidelines is discussed using this case. Management of the comorbidities is also discussed.

Keywords: Case discussion, dilated cardiomyopathy, heart failure

How to cite this article:
Dambalkar A. A case of dilated cardiomyopathy. J Pract Cardiovasc Sci 2017;3:163-5

How to cite this URL:
Dambalkar A. A case of dilated cardiomyopathy. J Pract Cardiovasc Sci [serial online] 2017 [cited 2023 Jun 4];3:163-5. Available from: https://www.j-pcs.org/text.asp?2017/3/3/163/224492

  Case Presentation Top

A 54-year-old gentleman was diagnosed to have dilated cardiomyopathy at the age of 50 years. He had shortness of breath for 1 year. On evaluation, he was found to have severe left ventricular (LV) dysfunction.

  Presenting Complaints Top

  • Worsening of shortness of breath
  • Unable to walk 100 m/take bath on his own for the past 2 months.

  Vitals Top

  • Pulse rate – 100/min
  • Blood pressure (BP) – 110/80 mmHg
  • Respiratory rate – 30/min.

  General Physical Examination Top

On general physical examination, the following were found:

  • Pedal edema +
  • Pallor/icterus/cyanosis/clubbing: Absent
  • Jugular venous pressure raised
  • Electrocardiography – Sinus tachycardia
  • Two-dimensional echo – Global hypokinesia
  • Severe LV dysfunction (LV ejection fraction [LVEF]) – 20%.

  Biomarkers Top

  • Brain natriuretic peptide (BNP) – 1000 pg/ml (<100 pg/ml)
  • Serum ST-2 60 ng/ml (<35 ng/ml).

Renal functions and liver function tests were within normal limit.

  Treatment Given Top

The patient visited a cardiologist and he was started on the following medications at the first visit:

  • Digoxin
  • Angiotensin receptor-neprilysin inhibitor (ARNI)
  • Ivabradine
  • Spironolactone.

  Questions Top

Is the treatment appropriate?

The treatment should be based on the guidelines issued recently by the European Society of Cardiology (ESC) and American Heart Association.[1],[2],[3],[4],[5],[6],[7]

According to the recent evidence from DIG trial, there is no mortality benefit from digoxin except for the rate of hospitalization which decreases but the downside of the drug is its propensity to cause ventricular arrhythmia leading to sudden cardiac death. In the current era of potent drugs against heart failure (HF), digoxin has minimal role.

ARNI is the most recent drug in the armamentarium of HF. The drug has been shown to successfully influence the outcome in patients with HF with low ejection fraction. The drug has been given Class I indication; however in the largest trial, PARADIGM HF, this drug was administered to patients tolerating angiotensin-converting enzyme inhibitors (ACEIs) and patients with hyperkalemia were excluded and New York Heart Association (NYHA) IV patients represented only 0.8% of the cohort. In the index patient, potassium levels should be checked. ACEI/angiotensin receptor blocker (ARB)-naïve patients are at a risk of angioedema and hypotension which can be life threatening. Although the evidence is in favor of ARNI, caution should be exercised in starting and monitoring the side effects of this group of drugs. According to the ESC guidelines, the patients should be first started on ACEIs, and if still symptomatic, they should be switched to ARNI while the American guidelines suggest that patients with HF can be started on ARNI directly.

Betablockers have not been started in the index patient. Carvedilol, metoprolol, and bisoprolol have strong evidence for improving the mortality and morbidity due to HF and are given Class I indication for patients with severe LV dysfunction. These drugs should be started in all patients with LVEF <45% and avoided only in patients with atrioventricular (AV) block. These three betablockers are relatively selective drugs and can be given safely in patients with Chronic obstructive airway disease (COAD) and peripheral artery disease except in patients with trifascicular block/2nd or 3rd degree AV block without pacemaker.

Ivabradine is not a first-line drug for HF and was given inappropriately in the index case. Patients whose symptoms are not controlled with betablockers and whose heart rate (HR) is above 70 beats per min (bpm) in spite of maximally tolerated or recommended dose are benefited by ivabradine.

How useful are biomarkers (brain natriuretic peptide and ST2) in the diagnosis and prognosis of patients? Do they help in the treatment of heart failure?

Low BNP helps to essentially rule out HF with a high negative predictive value; however, patients with high BNP levels need further evaluation due to low positive predictive value (0.4–0.6) in both acute HF (AHF) and nonAHF. Therefore, the use of NPs is recommended for ruling out HF, but not to establish the diagnosis. Unexpectedly, low levels of NPs can be detected in some patients with decompensated end-stage HF, flash pulmonary edema, or right-sided AHF which should be kept in mind while interpreting the results. NPs also have been used as adjuncts in monitoring therapeutic response to HF. In a study by Bayes Genis et al., patients with AHF were serially monitored with BNP levels which correlated significantly with symptom resolution. ARNI increases BNP levels as they are a substrate of neprilysin but not NT-proBNP levels and hence BNP should not be used in monitoring patients on ARNI.

Due to the absence of clear and consistent evidence for improvement in mortality and cardiovascular outcomes, there is insufficient data to inform specific guideline recommendations related to NP-guided therapy or serial measurements of BNP or NT-proBNP levels for the purpose of reducing hospitalization or deaths in the present document.

Cardiac troponin levels may be elevated in the setting of chronic or acute decompensated HF, suggesting myocyte injury or necrosis. Elevations in either troponin I or T levels in the setting of AHF are of prognostic significance but must be interpreted in a clinical context as it is also significantly raised in acute coronary syndrome.

ST2 is a member of the interleukin 1 receptor family, also known as interleukin 1 receptor-like 1. ST2 stands for “suppression of tumorigenicity 2.” ST2 is the most promising biomarker according to recent studies. Although not a diagnostic marker, ST2 may be useful in the risk stratification of patients with HF. In PRIDE study, ST2 was associated with a twofold increase in the risk of mortality regardless of other parameters, including NP. ST2 assessment was performed well in HF patients with both reduced (HFrEF) and preserved ejection fraction (HFpEF).

What is the role of ivabradine in this patient? When should we use it?

Ivabradine is a relatively new drug used to reduce sinus rate by acting on funny channels. High resting HR is an important and potentially modifiable risk factor in patients with HF. The SHIFT study suggested that ivabradine was beneficial when added to conventional treatment including a beta-blocker in HF patients in sinus rhythm whose resting HRs remained 70 bpm or greater and who had worse than moderate LV impairment.

Patients whose disease is not controlled with beta-blockers and whose HR is above 60 bpm are benefited by ivabradine. It is not a first-line drug for HF and was given inappropriately in the index case.

Our latest drug in the battle against heart failure is angiotensin receptor-neprilysin inhibitor/LCZ696. Where does angiotensin receptor-neprilysin inhibitor come in the management of heart failure?

Valsartan/sacubitril, an angiotensin-receptor/neprilysin inhibitor (ARNI), was approved on July 7 for patients with HFrEF. The approval was based on the PARADIGM-HF trial and came after an expedited review and fast-track designation by the FDA. The first effect is similar to the effect of ACEs and ARBs. The other effect strengthens a hormonal system regulated by BNP. BNP has multiple effects such as vasodilatation of blood vessels, natriuresis, as well as an increased diuresis. ARNIs are an option for those patients who continue having symptoms despite otherwise optimal treatment. In comparison to the ACEI enalapril, sacubitril/valsartan reduced the occurrence of the primary end point (cardiovascular death or hospitalization for HF) by 20% with a 16% reduction in all-cause mortality. These findings suggest that sacubitril/valsartan should replace an ACEI or ARB as the foundation of treatment of symptomatic patients (NYHA II–IV) with HFrEF (ACC Class I B). This is probably logical (if not entirely evidence based), as the lower risks of renal dysfunction and hyperkalemia with sacubitril/valsartan may enable more patients to achieve optimal renin-angiotensin aldosterone system inhibition. Despite the superiority of sacubitril/valsartan over enalapril in the PARADIGM-HF trial, some relevant safety issues remain when initiating therapy with this drug in clinical practice and it is the reason for the recommendation of ARNI by the ESC only a substitute to ACE/ARB if patient is persistently symptomatic on guideline-directed medical therapy.

Can we go beyond all these with metabolic modulation by altering the energy balance?

Metabolic modulators are a new class of drugs which benefit these patients by mainly altering the metabolism of heart without affecting the hemodynamics. These drugs increase glucose metabolism at the expense of free fatty acid, thereby enhancing efficient use of oxygen. Four potential metabolic modulators are trimetazidine, ranolazine, perhexiline, and etomoxir.

Trimetazidine is one of the established drugs in this group which directly blocks 3-ketoacyl coenzyme A thiolase, the key enzyme for fatty beta oxidation resulting in shift to glucose oxidation for energy. This shift is beneficial by providing more ATPs at the same oxygen consumption. It also improves endothelial function and reduces calcium overload and free radical injury. Four meta-analyses concluded that trimetazidine improves functional capacity and ejection fraction, delays and reverses remodeling, and reduces BNP in HF.

The patient comes back after 1 month and is in New York Heart Association II, ejection fraction 20%, blood pressure 110/70 mmHg, HB IS 9 gm/dl, K + 4.2 mmol/l, heart rate 90 bpm, and currently on metoprolol succinate 50 mg BD, ramipril 5 mg BD, and torsemide 20 mg OD. What to add at this stage and why?

The stage is set now for starting ARNI as the patient has tolerated ACEI and has potassium levels normal at baseline. ACEIs (ramipril) should be discontinued 36 h before starting ARNI. Patients with a history of angioedema and pregnant women should not be given ARNI. ARNIs should be started at a low dose (49/51 mg BD) and must be gradually uptitrated to 97/103 mg BD monitoring renal function after 1–2 weeks of every dose change.

Metoprolol succinate should be uptitrated gradually (double the dose at not <2 weeks) to decrease the HR to <70/min up to a maximum dose of 200 mg OD or split into two daily doses and patients should be monitored for hypotension or worsening HF due to negative inotropic effect of betablockers. In case patients are not able to tolerate high doses of betablockers and HR remains high (>70/min), ivabradine should be considered.

Diuretics (torsemide) should be titrated according to the symptoms and weight changes. Electrolytes and renal functions should be checked after 1–2 weeks of increase in dose.

Mineralocorticoid receptor antagonist is missing in the above treatment which is Class I indication for patients with LVEF ≤35%. Significant reduction in mortality (30%) and hospitalization rate (35%) in patients with HFrEF was shown in RALES and EMPHASIS-HF trials. Spironolactone should be added to the above treatment at 25 mg OD and slowly uptitrated 4 weekly monitoring of renal function and potassium.

Patient has moderate anemia and should be evaluated for its cause. Iron profile should be done, and if iron levels are found to be low (serum ferritin <100 μg/L or ferritin between 100 and 299 μg/L with transferrin saturation <20%), they should be supplemented with intravenous iron (IIa). In CONFIRM-HF trial, intravenous iron supplementation was found to improve 6-min walk test. Routine supplementation of erythropoietin in patients with anemia was not found beneficial.

A wholesome approach to patients targeting not only the cardiac illness but also other comorbidities (chronic obstructive pulmonary disease and arthritis) decreases the readmission rates. Counseling the patients makes them equipped to monitor side effects of the drugs and helps them titrating the medications. Warning signs must be explained to patients before discharge which can prevent serious complications.

Conflicts of interest

There are no conflicts of interest.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Writing Committee Members, Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr., et al. 2016 ACC/AHA/HFSA focused update on new pharmacological therapy for heart failure: An update of the 2013 ACCF/AHA guideline for the management of heart failure: A Report of the American college of cardiology/American heart association task force on clinical practice guidelines and the heart failure society of America. Circulation 2016;134:e282-93.  Back to cited text no. 1
Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JG, Coats AJ, et al. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: The task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) Developed with the special contribution of the heart failure association (HFA) of the ESC. Eur Heart J 2016;37:2129-200.  Back to cited text no. 2
Heart Failure Society of America, Lindenfeld J, Albert NM, Boehmer JP, Collins SP, Ezekowitz JA, et al. HFSA 2010 comprehensive heart failure practice guideline. J Card Fail 2010;16:e1-194.  Back to cited text no. 3
Marwick TH. The viable myocardium: Epidemiology, detection, and clinical implications. Lancet 1998;351:815-9.  Back to cited text no. 4
Allman KC, Shaw LJ, Hachamovitch R, Udelson JE. Myocardial viability testing and impact of revascularization on prognosis in patients with coronary artery disease and left ventricular dysfunction: A meta-analysis. J Am Coll Cardiol 2002;39:1151-8.  Back to cited text no. 5
Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr., Colvin MM, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the Management of heart failure: A Report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines and the heart failure Society of America. J Card Fail 2017;23:628-51.  Back to cited text no. 6
Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr., Drazner MH, et al. 2013 ACCF/AHA guideline for the management of heart failure: Executive summary: A report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Circulation 2013;128:1810-52.  Back to cited text no. 7


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