Heart Disease 4

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Although initial studies suggested that determination of BNP or N-terminal (NT) pro-BNP levels might be

useful for screening, the positive predictive value (PPV) for these tests in a low-prevalence and
asymptomatic population to detect cardiac dysfunction varies among studies, and the possibility of
false-positive results has significant costeffectiveness implications. Patients who are at very high risk of a
developing cardiomyopathy (e.g., those with a strong family history of cardiomyopathy or those
receiving cardiotoxic interventions; see Chapters 80 and 81) are appropriate targets for more aggressive
screening such as two-dimensional echocardiography to assess LV function. The STOP-HF (St. Vincent's
Screening To Prevent Heart Failure) showed that, in patients with known CV risk factors, screening with
BNP testing followed by collaborative care between internists and CV specialists resulted in a significant
reduction in LV dysfunction (odds ratio [OR], 0.55; 95% CI, 0.37 to 0.82; P = .003). Although there was no
significant reduction in clinical HF events, there was a significant decrease in the incidence rates of
emergency hospitalization for major CV events. 13 However, the routine periodic assessment of LV
function in low-risk patients is not currently recommended. Several sophisticated clinical scoring systems
have been developed to screen for HF in population-based studies, including the Framingham Criteria,
which screen for HF on the basis of clinical criteria, and the National Health and Nutrition Examination
Survey (NHANES), which uses selfreporting of symptoms to identify HF patients (Table 25.4). However, as
discussed in Chapter 21, additional laboratory testing is usually necessary to make a definitive diagnosis
of HF when these methodologies are used. TABLE 25.4 Diagnostic Criteria for Heart Failure (HF) in
Population-Based Studies FRAMINGHAM CRITERIA Major Criteria Minor Criteria Major or Minor Criteria
Paroxysmal nocturnal dyspnea or orthopnea Neck vein distention Rales Cardiomegaly Acute pulmonary
edema S3 gallop Increased venous pressure >16 cm H2O Hepatojugular reflux Ankle edema Night cough
Dyspnea on exertion Hepatomegaly Pleural effusion Vital capacity decreased One-third from maximal
capacity Tachycardia (rate >120/min) Weight loss >4.5 kg in 5 days in response to treatment NHANES
CRITERIA Category Criteria Score History Dyspnea: When hurrying on a hill 1 When walking at an
ordinary pace 1 Do you stop for breath when walking at an ordinary pace? 2 Do you stop for breath
when after 100 yards on flat ground? 2 Physical examination Heart rate: 91-110 beats/min 1 >110
beats/min 2 Jugular venous pressure (> 6 cm H2O): Alone 1 PLUS hepatomegaly or edema 2 Rales:
Basilar crackles 1 Crackles more than basilar crackles 2 Chest radiograph Upper zone flow redistribution
1 Interstitial pulmonary edema 2 Interstitial edema plus pleural fluid 3 Alveolar fluid plus pleural fluid 3

Heart failure (HF) is a condition where the heart's ejection performance declines after an initial index
event, leading to a decline in heart function. Left ventricular dysfunction (LV) can develop transiently in
various clinical settings, and it is crucial to recognize the relationship between LV dysfunction and the
clinical syndrome of HF.

LV dysfunction with pulmonary edema may develop acutely in patients with previously normal LV
structure and function, most frequently after cardiac surgery, severe brain injury, or systemic infection.
The general pathophysiologic mechanism involved is either stunning of functional myocardium or
activation of proinflammatory cytokines capable of suppressing LV function. Emotional stress can also
precipitate severe, reversible LV dysfunction accompanied by chest pain, pulmonary edema, and
cardiogenic shock in patients without CAD (takotsubo syndrome).

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