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 Table of Contents  
CASE BASED REVIEW
Year : 2022  |  Volume : 8  |  Issue : 2  |  Page : 79-83

Clinical evaluation of heart failure: A clinical case discussion of a patient with rheumatic heart disease


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

Date of Submission12-Jul-2022
Date of Acceptance15-Jul-2022
Date of Web Publication19-Aug-2022

Correspondence Address:
Mohsin Raj Mantoo
7th Floor, Cardiothoracic Sciences Centre, All India Institute of Medical Sciences, New Delhi - 110 029
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpcs.jpcs_29_22

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  Abstract 


A 44-year-old male with no prior cardiovascular risk factors presented with exertional dyspnea and dry cough followed by features of the right heart failure including early satiety and pedal edema. He had congestive heart failure at presentation with cardiac auscultation revealing murmurs of mitral regurgitation at the apex and tricuspid regurgitation at the lower left sternal border and aortic stenosis at the right second intercostal space. He was diagnosed as case of rheumatic heart disease based on clinical and echocardiographic assessment. The following clinical case discussion highlights some common questions that come to mind during evaluation of such patients. Physical examination findings in a patient presenting with heart failure syndrome are highlighted in particular.

Keywords: Heart failure, physical examination, rheumatic heart disease


How to cite this article:
Mantoo MR, Sharma V, Chaudhary S, Seth S. Clinical evaluation of heart failure: A clinical case discussion of a patient with rheumatic heart disease. J Pract Cardiovasc Sci 2022;8:79-83

How to cite this URL:
Mantoo MR, Sharma V, Chaudhary S, Seth S. Clinical evaluation of heart failure: A clinical case discussion of a patient with rheumatic heart disease. J Pract Cardiovasc Sci [serial online] 2022 [cited 2022 Oct 5];8:79-83. Available from: https://www.j-pcs.org/text.asp?2022/8/2/79/354135




  Introduction Top


The following case was discussed in a bedside class at our hospital and the same is presented in this manuscript. Special attention is provided to the physical examination findings in a patient presenting with the syndrome of heart failure.


  Clinical Case Top


A 44-year-old male, resident of Bihar, laborer by occupation, with no prior comorbidities, presented with complaints of dyspnea on exertion and dry cough for the past 3 months. Dyspnea was insidious in onset and progressed from New York Heart Association (NYHA) II to III over the next 1 month, not associated with orthopnea but associated with paroxysmal nocturnal dyspnea and nocturnal dry cough. One month after the onset of dyspnea, he developed bloating and early satiety, along with swelling of both the feet and loss of appetite. There was no history of exertional chest pain or syncope. There was no significant medical history and family history.

On examination, there was tachycardia (heart rate 102/min) with normal blood pressure (118/72 mmHg). He had pallor and mild pitting pedal edema, but no icterus, clubbing, or lymphadenopathy. Jugular venous pressure (JVP) was elevated (9 cm above the sternal angle [SA]) with prominent v wave and y descent. Cardiovascular system examination revealed suprasternal and neck pulsations on inspection with the apical impulse displaced to the left 7th intercostal space in the anterior axillary line, seen over more than one intercostal space. On palpation, there was a systolic thrill over both the carotids. On auscultation, a high pitched pansystolic grade 3/6 murmur was heard at the apex and radiating to the axilla, best heard with the diaphragm of the stethoscope, with the patient in the left lateral position and breath held in expiration. A holosystolic grade 3/6 murmur was also heard in the right 3rd and 4th intercostal spaces, best heard with the diaphragm of the stethoscope, radiating to the right parasternal area, and increasing in intensity with deep inspiration. A crescendo-decrescendo systolic murmur was also present with maximum intensity over the left 3rd intercostal space, radiating to the right 2nd intercostal space and both carotids, heard best with the diaphragm of the stethoscope, and the patient leaning forward. Hepatomegaly was present, with the lower border of liver palpable 3 cm below the right costal margin in the mid-clavicular line.


  Discussion Top


What is the New York Heart Association classification?

NYHA classification of heart failure, now more than a century old, is a subjective assessment (by the patient and the physician) of limitation of physical activity caused by heart failure.[1],[2] The NYHA classification is presented in [Table 1].
Table 1: New York Heart Association (NYHA) classification of heart failure

Click here to view


While the classification is over 100 years old and deeply engrained in the literature, its limitations have also been highlighted.[3] In a recent analysis of data from four randomized trials of heart failure, NYHA class had a poor correlation with mortality and other objective measures of functional limitation.[4]

What is the Canadian cardiovascular society grading for Angina?



Is cough a symptom of cardiac disease?

Cough is a reflex event mostly triggered by neural inputs from the airways or respiratory tract. However, it is well known that vagal stimulation from extra pulmonary structures such as esophagus or ear can also trigger the cough reflex. Cardiac conditions including heart failure syndrome and arrhythmias produce hemodynamic disturbances in the pulmonary circulation and congestion of interstitial spaces surrounding the airways which stimulates the vagal afferents triggering the cough reflex.[5] Cardiac cough is more likely to occur in supine posture and during night (conditions that increase pulmonary venous pressures). Nocturnal cough and wheezing are mentioned as “less typical” symptoms of heart failure in the European heart failure guidelines.[6]

What is the likely cause of right heart failure symptoms in the patient?

The most common cause of right heart failure is the increased right ventricular afterload caused by pulmonary hypertension due to left-sided heart failure.[7]

What are the cardiac causes of dyspnea in this 44-year-old patient?

Given the relatively rapid progression of heart failure symptoms (over a course of 3 months), I would like to consider following causes:

  1. Valvular heart disease, likely a regurgitant left sided valve lesion
  2. Dilated cardiomyopathy with decompensation
  3. Ruptured sinus of Valsalva aneurysm (Absence of chest pain is against this differential).


Can the patient have ischemic heart disease?

The patient is a middle-aged man with no cardiovascular risk factors (No known hypertension, diabetes, dyslipidemia, smoking or family history of premature atherosclerotic cardiovascular disease), and no history of typical angina. However, given the predisposition of South Asians to earlier onset of coronary artery disease (CAD), we may consider a noninvasive coronary evaluation if there is a suspicion of CAD after detailed patient evaluation. The European guidelines on stable CAD (or chronic coronary syndromes) endorse the assessment of pretest probability of CAD in patients with angina or dyspnea.[8] Our patient has pretest probability between 5% and 15% and guidelines suggest that CAD testing may be considered after assessing the overall clinical picture including the presence of CAD risk factors, electrocardiography (ECG) changes, echocardiographic markers (like regional wall motion abnormalities), or presence of coronary calcium on computed tomography (CT).

What are the usual precipitating factors of decompensation in a chronic heart failure patient?

Factors precipitating decompensation and heart failure hospitalization include myocardial ischemia/infarction, arrhythmias, uncontrolled hypertension, pneumonia, worsening renal function, nonadherence to diet or medications, or anemia.[9]

If the valvular heart disease in this patient is rheumatic, can acute rheumatic activity explain his symptoms?

Patients of rheumatic heart disease are at risk of recurrences of acute rheumatic fever (ARF). However, ARF is uncommon/rare after 25–30 years of age.[10],[11]

Can this be a presentation of myocarditis?

Myocarditis should be in the list of differential diagnoses of a new onset heart failure patient, especially in presence of raised biomarkers of myocardial injury, segment changes (ST)-T changes in the ECG, left ventricular (LV) dysfunction on echocardiogram, and absence of CAD. Myocarditis is mostly triggered by viruses, though other infectious agents, drugs/toxins, and systemic immune mediated inflammatory disorders can also cause myocarditis.[12] What is not completely understood is the fact that only a subset of patients with viral myocarditis are not able to clear the virus or silence the inflammatory response with resulting chronic inflammatory cardiomyopathy.[13] The prodromal symptoms of a viral infection such as fever, myalgias, or decreased appetite may not be present in all patients and cannot be relied on for accepting or rejecting a diagnosis of myocarditis.

What are the points in favor of ruptured sinus of valsalva aneurysm?

RSOV typically occurs in middle aged individuals (more common in males) and usually (but not always) presents with acute chest pain which is followed by the clinical syndrome of heart failure. The characteristic continuous murmur raises the suspicion of RSOV in such cases.[14],[15]

Comment on the patient's jugular venous pressure?

JVP was estimated from the right internal jugular vein pulsations observed in the neck with the patient's head-end raised approximately 30 degrees. The upper most point of pulsations was 9 cm from the SA with prominent y descent. Kussmaul sign was absent.

What are the clinical implications of raised jugular venous pressure?

JVP directly estimates right atrial pressure. Interestingly, from the data of ESCAPE trial, raised JVP also correlated with raised pulmonary capillary wedge pressure (PCWP).[16] There are data to suggest that elevated JVP is independently associated with increased risk of death or hospitalization due to heart failure.[17] Therefore, JVP is not only a marker of fluid status (congestion) but also a predictor of adverse HF outcomes.

Why do we take sternal angle for measuring the height of jugular venous pressure?

The classic teaching is to measure the distance between SA and the top-most point of jugular venous pulsations and add 5 cm to it, assuming the distance between the SA and the mid-right atrium (RA) as 5 cm in all patients. However, in an interesting study, using CT scans in 160 patients, the SA-RA distance was measured in different positions and the authors concluded that the distance actually varied extensively between patients and with patient position.[18]

What is the role of hepato jugular reflux?

Hepatojugular reflux (HJR) refers to a rise in JVP by >3 cm which is sustained for at least 10 s of continuous mid-abdominal compression followed by abrupt fall.[19] A positive HJR implies increased ventricular filling pressures. In absence of isolated RV failure, positive HJR correlates with a PCWP of ≥15 mmHg.[20] Positive HJR also portends a worse outcome in patients of HF including increased risk of death.[19]

What is pseudo collapsing pulse of mitral regurgitation (MR) ?

In acute mitral regurgitation (MR) or end stage chronic severe MR, a sudden decrease in forward flow (forward stroke volume) late in systole results in arterial pulse falling off rapidly, giving an impression of collapsing or bounding pulse even if the pulse pressure is normal.

What are the auscultatory characteristics of mitral regurgitation murmur?

MR most commonly produces a holosystolic murmur, but in certain instances can produce an early systolic (e.g., acute MR) or late systolic murmur (e.g., mitral valve prolapse [MVP]) or holosystolic murmur with mid-systolic accentuation (e.g., rheumatic MR). The murmur of MR is usually high pitched, heard best with the diaphragm of the stethoscope at the cardiac apex with patient in the left lateral decubitus position. In general, the intensity of murmur is Grade III or less (so thrill is less common in MR). If the MR jet is directed posteriorly, then the murmur radiates toward the left axilla (most common) and if it is directed more anteriorly, then it radiates toward the base where it may be confused with the murmur of aortic stenosis or hypertrophic obstructive cardiomyopathy.[21] Murmur of MR generally has no respiratory variation and may decrease in intensity with standing or Valsalva maneuver. Certain conditions may decrease the intensity of MR murmur including LV dysfunction, low output states, huge left atrium (LA) size, or associated mitral stenosis.

In acute MR, the rapid increase of LA pressure and equalization of LV to LA pressure gradient restricts the regurgitation to early systole, that is, an acute MR produces a decrescendo early systolic murmur.[22] In MVP, the murmur is preceded by a mid-systolic click followed by a late systolic murmur.[23] The murmur of MVP is unique in that it increases in intensity with standing and Valsalva maneuver. Conversely, passive leg raising, isometric handgrip, and squatting reduce the intensity of murmur in MVP (click occurs later and the intensity of murmur decreases).

What is the second heart sound (S2) like in severe magnetic resonance?

In a significant MR, there is reduced forward stroke volume and ejection time, resulting in an earlier A2 and hence wide splitting of S2.

What is the significance of third heart sound (S3) in magnetic resonance?

S3 is common in patients with hemodynamically significant mitral regurgitation, but it does not necessarily mean LV systolic dysfunction or elevated filling pressures.[24]

What is your final diagnosis after history and physical exam?

  • Rheumatic heart disease
  • Severe mitral regurgitation
  • Severe aortic stenosis
  • Moderate tricuspid regurgitation
  • Congestive heart failure
  • Pulmonary venous hypertension
  • NYHA III
  • Normal sinus rhythm
  • Anemia.


Describe the ECG findings in the patient

The given ECG [Figure 1] has normal sinus rhythm and QRS axis with evidence of LV hypertrophy. There is no evidence of any right or left atrial abnormality. There are no significant ST-T abnormalities.
Figure 1: 12 lead electrocardiogram of the patient

Click here to view


Describe the echocardiographic findings of the patient

The echo [Figure 2]a and [Figure 2]b is an apical 4-chamber view with near normal biventricular function. The mitral valve leaflets are thickened and posterior leaflet is fixed. On color flow, there is severe mitral regurgitation.
Figure 2: 2D Echocardiographic images of the patient. (a) Apical 4-chamber view; (b) Color flow doppler across mitral valve; (c) Color flow doppler across aortic valve (d) Continuous wave doppler across aortic valve

Click here to view


The next echo [Figure 2]c and [Figure 2]d is an apical 5-chamber view with thickened aortic valve leaflets (with no calcium) along with restricted opening. On color flow, there is turbulence of flow across the aortic valve along with mild aortic regurgitation jet. Continuous wave Doppler fits the criteria for severe aortic stenosis with peak velocity 4.75 m/s and mean gradient 54 mmHg.

Acknowledgment

The authors would like to thank Professor SC Manchanda, Former Head of Department of Cardiology, AIIMS, who conducted this case discussion.

Patient consent

Was taken for publication of this case discussion.

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 understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Raphael C, Briscoe C, Davies J, Ian Whinnett Z, Manisty C, Sutton R, et al. Limitations of the New York heart association functional classification system and self-reported walking distances in chronic heart failure. Heart 2007;93:476-82.  Back to cited text no. 3
    
4.
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Grabczak EM, Stec S, Dabrowska M, Plevkova J, Krenke R. Cough as a cause and consequence of heart dysfunction – Current state of Art. Physiol Res 2020;69:S105-21.  Back to cited text no. 5
    
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McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Böhm M, et al. 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021;42:3599-726.  Back to cited text no. 6
    
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Konstam MA, Kiernan MS, Bernstein D, Bozkurt B, Jacob M, Kapur NK, et al. Evaluation and management of right-sided heart failure: A scientific statement from the American heart association. Circulation 2018;137:e578-622.  Back to cited text no. 7
    
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Fonarow GC, Abraham WT, Albert NM, Stough WG, Gheorghiade M, Greenberg BH, et al. Factors identified as precipitating hospital admissions for heart failure and clinical outcomes: Findings from OPTIMIZE-HF. Arch Intern Med 2008;168:847-54.  Back to cited text no. 9
    
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Spinetto H, Lennon D, Horsburgh M. Rheumatic fever recurrence prevention: A nurse-led programme of 28-day penicillin in an area of high endemnicity. J Paediatr Child Health 2011;47:228-34.  Back to cited text no. 10
    
11.
Kumar RK, Antunes MJ, Beaton A, Mirabel M, Nkomo VT, Okello E, et al. Contemporary diagnosis and management of rheumatic heart disease: Implications for closing the gap: A scientific statement from the American heart association. Circulation 2020;142:e337-57.  Back to cited text no. 11
    
12.
Tschöpe C, Cooper LT, Torre-Amione G, Van Linthout S. Management of myocarditis-related cardiomyopathy in adults. Circ Res 2019;124:1568-83.  Back to cited text no. 12
    
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Tschöpe C, Ammirati E, Bozkurt B, Caforio AL, Cooper LT, Felix SB, et al. Myocarditis and inflammatory cardiomyopathy: Current evidence and future directions. Nat Rev Cardiol 2021;18:169-93.  Back to cited text no. 13
    
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Parashar. Ruptured Sinus of Valsalva aneurysm: Clinical Case Presentation and Management. Available from: https://www.j-pcs.org/article.asp?issn=2395-5414;year=2017;volume=3;issue=2;spage=109;epage=114;aulast=Parashar.  Back to cited text no. 14
    
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Moreels S. Ruptured Sinus of Valsalva in an Asymptomatic patient - A Case Report European Cardiology 2012;8:139-41.  Back to cited text no. 15
    
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Drazner MH, Hellkamp AS, Leier CV, Shah MR, Miller LW, Russell SD, et al. Value of clinician assessment of hemodynamics in advanced heart failure: The escape trial. Circ Heart Fail 2008;1:170-7.  Back to cited text no. 16
    
17.
Drazner MH, Rame JE, Stevenson LW, Dries DL. Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure. N Engl J Med 2001;345:574-81.  Back to cited text no. 17
    
18.
Seth R, Magner P, Matzinger F, van Walraven C. How far is the sternal angle from the mid-right atrium? J Gen Intern Med 2002;17:852-6.  Back to cited text no. 18
    
19.
Thibodeau JT, Drazner MH. The role of the clinical examination in patients with heart failure. JACC Heart Fail 2018;6:543-51.  Back to cited text no. 19
    
20.
Ewy GA. The abdominojugular test: Technique and hemodynamic correlates. Ann Intern Med 1988;109:456-60.  Back to cited text no. 20
    
21.
Perloff JK, Harvey WP. Auscultatory and phonocardiographic manifestations of pure mitral regurgitation. Prog Cardiovasc Dis 1962;5:172-94.  Back to cited text no. 21
    
22.
Ronan JA Jr., Steelman RB, DeLeon AC Jr., Waters TJ, Perloff JK, Harvey WP. The clinical diagnosis of acute severe mitral insufficiency. Am J Cardiol 1971;27:284-90.  Back to cited text no. 22
    
23.
Hutter AM Jr., Dinsmore RE, Willerson JT, DeSanctis RW. Early systolic clicks due to mitral valve prolapse. Circulation 1971;44:516-22.  Back to cited text no. 23
    
24.
Folland ED, Kriegel BJ, Henderson WG, Hammermeister KE, Sethi GK. Implications of third heart sounds in patients with valvular heart disease. The veterans affairs cooperative study on valvular heart disease. N Engl J Med 1992;327:458-62.  Back to cited text no. 24
    


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