Background: Peripheral muscle electrostimulation (PME), including neuromuscular electrical stimulation (NMES) and functional electrical stimulation (FES), has been increasingly acknowledged as an effective adjunctive or complementary treatment to voluntary exercise in elderly cardiac patients who cannot perform sufficient amounts of voluntary exercise, with limited research on optimal protocols. Sarcopenia, defined as a progressive decrease in muscle mass, strength and function, affects approximately 34% of heart failure (HF) patients and considerably worsens their prognosis. The objective of this systematic review is to summarize the current evidence on the theoretical mechanisms, physiological pathways, safety and efficacy of PME in older adults within a cardiac rehabilitation (CR) setting with a specific emphasis towards sarcopenia reversal. Methods: We performed a systematic review following PRISMA 2020 guidelines. A systematic search of the PubMed, Embase, Cochrane Library, CINAHL and PEDro databases from inception until December 2025 was conducted. We searched for randomized controlled trials (RCTs) and controlled clinical trials focusing on PME in patients with cardiac diseases aged 65 years or older. The main outcomes were physical function (assessed with the Short Physical Performance Battery [SPPB] and 6-minute walk distance [6MWD]), muscle strength, muscle mass, and safety. The Cochrane Risk of Bias tool was used for quality evaluation of the studies. Results: Eight studies were included, with 387 participants and mean age between 78 to 85 years. PME consistently improved lower extremity muscle strength (MD: 5.2% body weight, 95% CI = 1.2–9.1, p = 0.013) along with SPPB scores ranging from +2.3 to +2.67 points (all p < 0.05). Home-based NMES achieved 100% adherence rates and no cardiovascular adverse events were reported. The mechanisms by which PME is beneficial involve peripheral skeletal muscle adaptations without eliciting central hemodynamic stress, increased endothelial function, aerobic enzyme activity, protein anabolism stimulation and muscle proteolysis inhibition. No significant effects were observed on BNP levels, hospital readmissions or mortality. PME has been shown to attenuate the progression of sarcopenia through hypertrophy of type I and II muscle fibers, as well as mitochondrial biogenesis. Conclusions: PME is a safe, feasible adjunct to conventional CR in frail elderly cardiac patients, particularly those with exercise intolerance and sarcopenia. It improves peripheral muscle function, physical performance, and muscle protein balance without cardiovascular stress. Larger multicenter trials are needed to establish optimal protocols and long-term clinical outcomes. Registration: PROSPERO CRD420261347748 (protocol registered prior to data extraction).