In outpatients with stable CAD, we found that either a PHQ-2 cutpoint of ≥2 or a PHQ-9 cutpoint of ≥6 optimized combined sensitivity and specificity for detecting MDD based on a structured clinical interview. A two-step screening approach using both instruments had similar overall diagnostic accuracy to using either alone. As compared with a structured clinical interview for MDD, a “PHQ diagnosis” using the PHQ-9 responses to diagnose MDD was highly specific, but resulted in many false negatives.
Our results build on the work of Stafford et al. who examined a group of individuals in Australia 3 months after discharge from hospitalization for an acute MI or a coronary revascularization procedure.13
They also found that a PHQ-9 cutoff score of ≥6 optimized sensitivity and specificity. We added to this work by demonstrating that the PHQ-2 performs similarly to the PHQ-9 and that two-step screening with the PHQ-2 followed by the PHQ-9 does not improve results compared to screening with either the PHQ-2 or the PHQ-9 alone. An obvious benefit to using the PHQ-2 is its relative brevity. On the other hand, the PHQ-9 may be a better tool for tracking depressive symptoms over time.
We generated cutoff scores that optimized the balance between sensitivity and specificity. In clinical settings, scores can be used to assess depression severity, to monitor the efficacy of treatment, or to identify patients likely to have a diagnosis of MDD based on further assessment. Cutoff points can also be used for research purposes, but not for the formal diagnosis of MDD. A formal diagnosis of MDD requires a clinical interview that assesses specific symptom patterns, as well as evidence of functional limitations.
As demonstrated in primary care settings, improved depression outcomes are likely to occur only when a collaborative care model is used, including the use of evidence-based protocols for treatment, active collaboration between primary care providers and mental health specialists, active monitoring of adherence to therapy, and access to structured psychotherapy.17
In the absence of these services, there is no evidence that screening alone is of benefit to patients in CVD settings. It must be noted, however, that this conclusion is made from the perspective of depression care alone and does not take into account the possibility that depression screening may have other potential benefits to patients with CVD. Many studies have now shown that patients with positive depression screens are at increased risk of cardiovascular morbidity and mortality.18
If depression screening identifies a group of high-risk patients who derive particular benefit from certain cardiac procedures or from interventions focused on enhancing adherence to medication or to secondary prevention behaviors, for example, then screening may be useful in therapeutic decision making even in the absence of mechanisms for formal depression diagnosis, treatment, and follow-up.
It must also be noted that this analysis is based on data from a study of outpatients with stable CAD, and the degree to which conclusions generalize to patients hospitalized with acute coronary syndromes is unknown. Furthermore, since only 7% of eligible patients actually enrolled in the study, results may not generalize well to other groups of CAD patients, although this response rate is comparable to other large cohort studies, such as the Coronary Artery Disease in Young Adults Study and the Cardiovascular Health Study.19,20
Additional research is needed on screening in acute care settings. Studies are also needed that examine paradigms, such as multiple positive screens prior to initiating formal evaluation, with the goal of reducing the high number of false positives generated in initial screening. Furthermore, clinical management paradigms are needed to establish whether screening in cardiovascular care settings leads to net benefits for patients.