When you break the news to a patient that he/she has heart failure they are usually very upset. The diagnosis carries the connotation of imminent death. The result is that doctors will use an euphemism and say something like ” You have water in your lungs or you have too much salt and water on your ankles”. This usually impresses them that the doctor has picked up their disease and they will happily go home without undue fear. They will conscientiously drink less water and eat less salt …not withstanding that advanced heart failure is a cause of hyponatremia which carries a very bad prognosis. So when do we as clinicians diagnose heart failure? It is a clinical diagnosis; remember fatigue and dyspnoea should alert you that something is wrong. Previous symptoms are also important.
So how does the American College of Cardiology/American Heart Association (ACC/AHA) stage heart failure?
Stage A. At high risk for HF but without structural heart disease or symptoms of HF. These people need monitoring and treatment of or reduction in possible etiological factors like hypertension, obesity, diabetes etc.
Stage B. Structural heart disease without current or prior signs or symptoms of HF. More frequent monitoring is required as well as prophylactic treatment like antiplatelet drugs etc.
Stage C. Structural heart disease with prior or current symptoms of HF. These patients require active treatment and careful follow up.
Stage D. Refractory HF requiring specialized interventions. The drugs you have been using are not proving effective hence more active intervention is required.
What significance is given to the ejection fraction? The clinical syndrome of heart failure (HF) may develop in patients with any left ventricular ejection fraction (LVEF). Nearly half of patients with HF have an LVEF ≤40 percent (HF with reduced LVEF [HFrEF]), and nearly half have an LVEF ≥50 percent (HF with preserved LVEF [HFpEF]). The remaining 10 to 24 percent of patients with HF present with an LVEF falling in the intermediate range (41 to 49 percent) between these two extremes.
- Signs or symptoms suggestive of heart disease such as unexplained electrocardiographic abnormality, palpitations, stroke, or peripheral embolic event.
- When will you investigate left ventricular systolic function?
- Signs or symptoms of coronary artery disease. Assessment of regional and global LV systolic function is commonly combined with stress testing.
- The presence of ventricular arrhythmias is a common indication for evaluation of LV function and structure as part of an evaluation to determine whether there is a structural cause for the arrhythmia.
- If there are signs or symptoms of heart failure (HF) then information on LV systolic function as well as diastolic function, chamber geometry, regional wall motion, and valve function is important for diagnosis and management.
- Before starting potentially toxic therapy as in cancer chemotherapy.
- Evaluation prior to a procedure for which LV systolic dysfunction may be a risk factor or contraindication. As an example, a transthoracic echocardiogram (TTE) is performed in patients with suspected or increased risk of LV dysfunction prior to renal transplantation.
How can we assess left ventricular function? LVEF is not a reliable measure of contractility, and changes over time with or without treatment, may be impacted by blood pressure and valvular function, and also varies by the method used. The methods used are echocardiography, cardiovascular magnetic resonance (CMR), cardiac computed tomography, and radionuclide angiography) In addition, LVEF alone does not incorporate other potentially important metrics such as LV cavity size and whether systolic dysfunction is regional or global.
I am copying an article from Journal Watch to clarify (or confuse) the relationship between systolic and diastolic blood pressure.
July 17, 2019
Associations Between Systolic and Diastolic BP and Cardiovascular Outcomes
Allan S. Brett, MD and Harlan M. Krumholz, MD, SM reviewing Flint AC et al. N Engl J Med 2019 Jul 18
A large analysis found that both measurements were independent predictors of adverse outcomes.
Fifty years ago, diastolic blood pressure (BP) was thought to be more predictive of adverse cardiovascular (CV) events than systolic BP, but epidemiologic studies eventually overturned that idea. More recently, systolic BP has been deemed more important, although both systolic and diastolic BP targets are recommended in guidelines (NEJM JW Gen Med Dec 15 2017 and J Am Coll Cardiol 2018; 71:e127). Now, researchers have explored relations between BP and 8-year CV outcomes (myocardial infarction or stroke) in more than 1 million adults (median age, 53) from northern California’s Kaiser Permanente health system. The analysis used weighted averages of each person’s BP measurements (median, 22 measurements per person) during the 8-year observation period.
In multivariable analyses, systolic and diastolic BP were each associated independently with increased risk for CV events, but the effect was greater for systolic than for diastolic BP. For systolic BPs of 136 and 160 mm Hg, the predicted 8-year risks for a CV event were 1.9% and 4.8%, respectively. For diastolic BPs of 81 and 96 mm Hg, CV event rates were 1.9% and 3.6%, respectively. Relative risks for CV events (but not necessarily absolute risks) were similar regardless of use of antihypertensive medication. CV risk increased when diastolic BP was in the 60s or lower (i.e., a “J-curve” relation), but this relation disappeared with adjustment for age and other covariates.
Here is another study which is industry sponsored which shows that the prognosis in heart failure may not be etiology related.
July 10, 2019
Etiology and Treatment Response in Heart Failure with Reduced Ejection Fraction
Harlan M. Krumholz, MD, SM reviewing Balmforth C et al. JACC Heart Fail 2019 Jun Udelson JE. JACC Heart Fail 2019 Jun
In patients receiving contemporary guideline-based medical therapy, etiology does not influence outcomes.
The randomized, double-blind, industry-sponsored PARADIGM-HF trial (NEJM JW Cardiol Oct 2014 and N Engl J Med 2014; 371:993) reported the superiority of angiotensin receptor–neprilysin inhibitor (ARNI) treatment with sacubitril/valsartan to the angiotensin-converting-enzyme inhibitor enalapril in patients with chronic heart failure and heart failure with reduced ejection fraction (HFrEF). The current investigators reanalyzed these data to determine how the outcomes and treatment effect varied by the etiology of HFrEF.
The exclusion criteria for PARADIGM-HF included symptomatic hypotension or systolic blood pressure <100 mm Hg, estimated glomerular filtration rate <30 mL/minute/1.73 m2, and potassium >5.2 mmol/L. Of the 8933 participants, 60% had an ischemic etiology. Analyses adjusted for many prognostic factors. On the combined outcome (cardiovascular mortality or HF hospitalization), the adjusted hazard ratio did not differ between patients with ischemic etiology and those with hypertensive or idiopathic etiologies, the two most common causes of nonischemic HF. There was no evidence of an interaction between HF etiology and the effect of ARNI therapy. The benefit of ARNI therapy was consistent across HF etiologies.
In contrast with some prior study findings, this assessment of PARADIGM-HF shows that in a group largely treated with contemporary guideline-based medical therapy, etiology did not influence the outcome. This study had a more comprehensive risk adjustment than many others, including measurements of natriuretic peptides. Also, interestingly, the etiology had no effect on the treatment response.