SummaryBackground: Cocaine produces adverse cardiovascular effects, some of which cannot be explained by epicardial coronary artery disease (CAD) or spasm.Hypothesis: The hypothesis of this study was that cocaine users would have increased coronary microvascular resistance, even in the absence of recent myocardial infarction (MI), CAD, or spasm.Methods: Microvascular resistance was assessed by the corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (cTFC) method in a consecutive series of 59 cocaine users without acute or recent MI or angiographically significant epicardial stenosis (> 50%) or spasm. The cTFCs in these patients were compared with 21 normal controls and with published normal cTFC values.Results: The cTFC was significantly elevated (by 26-54%) in cocaine users. The cTFCs in the left anterior descending (LAD), circumflex (LCx), and right coronary (RCA) arteries in cocaine users were 30.0 ± 10.9, 34.1 ± 11.5, and 28.6 ± 11.8, respectively, compared with values in normal controls of 21.3 ± 4.3 (p = 0.001), 24.4 ± 7.2 (p = 0.001), and 22.7 ± 5.1 (p = 0.04), respectively, and published normal cTFC values (all p < 0.01). An abnormally high cTFC was present in 61% of patients in the LAD, 69% in the LCx, and 47% in the RCA.

Symptomatic Improvement was evaluated in 64 patients with drug-refractory atrial fibrillation or atrial flutter who underwent atrioventricular (AV) nodal ablation and permanent pacemaker implantation. The arrhythmias were chronic in 40 patients and paroxysmal in 24 patients. All were refractory to multiple drugs (3.7 +/- 1.5) and had severe symptoms: palpitations (58 patients), dyspnea (n=58), dizziness (n=38), asthenia (n=37), and chest pain (n=20). All underwent AV nodal ablation and single- (n=39) or dual-chamber (n=25) pacemaker implantation. During follow-up of 20.4 +/- 17.8 months, palpitations improved in 100% of 58 patients who had palpitations before the ablation, dyspnea improved in 75% of 58 patients, chest pain in 95% of 20 patients, asthenia in 75% of 37 patients, and dizziness in 93% of 38 patients. Moderate to significant improvement in these symptoms was reported in 83% of patients and mild improvement in 5%. Before ablation, 77% of patients were in New York Heart Association functional class III or IV. After ablation, 19% of patients were in the same functional classes (P < 0.05). Thus, AV nodal ablation and pacemaker implantation in patients with drug-refractory atrial fibrillation or flutter was associated with significant improvement in presenting symptoms and functional capacity. A randomized, controlled study is needed to compare this form of therapy with other therapeutic modalities.