Enhancing patient acceptance of ICD implantation through structured shared decision making: conversation is key.

BACKGROUND: Implantable cardioverter-defibrillators (ICDs) and cardiac resynchronization therapy defibrillators (CRT-D) are lifesaving treatments for patients at risk for sudden cardiac death. Effective physician-patient communication during the shared decision-making process is essential. Electrophysiologist-patient conversations were targeted to obtain objective data on the interaction, understand the conversation framework, and uncover opportunities for improved communication. METHODS: Individuals previously identified as requiring an ICD/CRT-D but declined implantation were recruited for this four-stage interview and survey-based study. Quantitative analysis of surveys and AI analysis of conversation videos was conducted to evaluate patient participant expectations, analyze feedback about the conversations with study physicians, and gauge willingness for device implantation. RESULTS: The study included 27 patients (mean age 51 years, 51.9% female) and 9 study physicians. Patients were significantly more willing to undergo ICD/CRT-D implantation after conversing with study physicians compared to their own physicians and pre-conversation surveys (mean scores: 5.0, 3.1, and 4.4 out of 7, respectively; p < 0.001). Patient participants had higher satisfaction with the study conversation, rating study physicians higher in effectiveness of explanations, responsiveness to questions, and overall quality of the conversation compared to their own physicians (all p < 0.001). CONCLUSIONS: In a cohort of patients who previously declined ICD/CRT-D implantation, patient satisfaction and willingness to undergo implantation of a guideline-directed device therapy increased significantly following a structured conversation with study physicians. Identified key elements could be integrated into user-friendly tools and educational materials to facilitate these conversations, improving patient engagement with the decision-making process and enhancing informed acceptance of indicated device therapies.

Sympathoexcitation is attenuated during low level lower body negative pressure in subjects who develop pre-syncope.

The purpose of this study was to compare the hemodynamic and sympathetic nerve activity (SNA) responses to graded lower body negative pressure (LBNP) in healthy subjects with either a positive (n = 24, SNA in 8) or a negative (n = 18, SNA in 6) LBNP response. A positive LBNP response was defined as an abrupt drop in systolic blood pressure associated with a decrease in heart rate and/or a decrease in SNA. All positive responses were accompanied by symptoms common to pre-syncope, defined as lightheadedness, diaphoresis, tunnel vision and/or nausea. If subjects tolerated 30 minutes of LBNP, this was considered a negative response. Comparisons were made between baseline, -10 mmHg (low-level LBNP) and -60 mmHg (high-level LBNP). Baseline SNA and arterial baroreflex sensitivity were not different between the 2 groups. However, subjects with pre-syncope had a significantly attenuated SNA response during low-level LBNP (p < 0.05) compared to subjects who did not experience pre-syncope. The hemodynamic data during high-level LBNP were similar until the occurrence of pre-syncope. Pre-syncope was preceded by a significant decrease in heart rate and SNA. Our findings suggest that subjects with LBNP induced pre-syncope might have an impairment in the cardiopulmonary baroreflex gain function in the setting of a preserved arterial baroreflex gain.

Serotonin reuptake inhibitor (Paxil) does not prevent the vasovagal reaction associated with carotid sinus massage and/or lower body negative pressure in healthy volunteers.

BACKGROUND: The purpose of this study was to assess the effect of the serotonin reuptake inhibitor paroxetine hydrochloride (Paxil, SmithKline Beecham) on cardiovascular reflexes. We hypothesized that Paxil prevents neurally mediated syncope (NMS) by attenuating the sympathoinhibition and vagotonia associated with a vasovagal reaction. METHODS AND RESULTS: In a double-blind randomized study, 25 healthy subjects with a positive response to either carotid sinus massage (CSM) or lower body negative pressure (LBNP) received Paxil (20 mg/d) or placebo for 6 weeks. Arterial baroreflex sensitivity (BRS), muscle sympathetic nerve activity (SNA), baroreflex control of SNA, blood pressure, and heart rate responses to CSM and LBNP were measured at baseline and at 6 weeks. Nineteen subjects completed the study (Paxil, n=9; placebo, n=10). In the Paxil group, BRS decreased significantly compared with baseline (15.8+/-4.0 ms/mm Hg versus 11.0+/-2.6 ms/mm Hg, P=0.05); however, all 9 subjects continued to have a positive response to LBNP with presyncope. Paxil did not attenuate the sympathoinhibition or vagotonia associated with a positive LBNP response and had no significant effect on baroreflex control of SNA. In the control group, no significant change in BRS was noted compared with baseline. Seven out of 9 subjects who had a positive LBNP response at baseline had a repeat positive LBNP response, and the subject with a positive CSM at baseline had a negative response at 6 weeks. CONCLUSIONS: Paxil decreases arterial BRS but does not prevent the presyncope associated with LBNP. The effect of Paxil on the autonomic reflexes in patients with neurally mediated syncope remains unclear.