Coronary Microcirculatory vasoconstriction during ischemia in patients with unstable angina

OBJECTIVE To verify the behavior of coronary microvascular tone during spontaneous ischemia in patients with unstable angina (UA). BACKGROUND In UA, the pathogenetic role of vasoconstriction is classically confined at the stenotic coronary segment. However, microcirculatory vasoconstriction has been also suggested by previous experimental and clinical studies. METHODS The study included 10 patients with UA (recent worsening of anginal threshold and appearance of angina at rest) and single-vessel CAD. Blood flow velocity was monitored by a Doppler catheter in the diseased artery. Transstenotic pressure gradient was monitored by aortic and distal coronary pressure monitoring. Stenosis resistance was calculated as the ratio between pressure gradient and blood flow, microvascular resistance as the ratio between distal pressure and blood flow. Measurements were obtained at baseline, following intracoronary adenosine (2 mg) and during transient ischemia. Aortic and distal coronary pressures were also measured during balloon coronary occlusion. RESULTS Adenosine did not affect stenosis resistance, while it decreased (p , 0.05) microvascular resistance to 52 6 22% of baseline. Angina and ischemic ST segment shift were associated with transient angiographic coronary occlusion in 7 of 10 patients; however, in no case was ischemia associated with interruption of flow. Despite markedly different flow values, distal coronary pressure was similar during adenosine and during spontaneous ischemia (48 6 15 vs. 46 6 20 mm Hg, respectively, NS). During ischemia, a marked increase in the resistance of both coronary stenosis and coronary microcirculation was observed (to 1,233% 6 1,298% and 671% 6 652% of baseline, respectively, p , 0.05). Distal coronary pressure was markedly reduced during balloon coronary occlusion (14 6 7 mm Hg, p , 0.05 vs. both adenosine and ischemia), suggesting the absence of significant collateral circulation. CONCLUSIONS In patients with UA, transient myocardial ischemia is associated with vasoconstriction of both stenotic arterial segment and downstream microcirculation

Does the combination with handgrip increase the sensitivity of dipyridamole-echocardiography test?

The aim of this study was to assess the possibility of increasing the sensitivity of dipyridamole-echocardiography testing (DET:2-D echo monitoring during dipyridamole infusion) by combining this procedure with handgrip testing. Dipyridamole-handgrip test (DHT) was therefore performed in 24 patients with rest/effort angina, negative DET, and negative handgrip-echo (without dipyridamole pretreatment). DHT consisted of 4.5 min of sustained 25% maximum grip strength, started 4 min after the end of dipyridamole infusion (0.56 mg/kg for 4 min). Interpretable studies were obtained in all patients. Of the 24 patients tested (10 without and 14 with significant coronary artery disease, CAD), only one CAD patient had a positive DHT, which indicates an increased sensitivity of 7% versus DET alone. In conclusion, DHT is feasible in all patients and--if compared to DET--has the same specificity. However, in spite of the theoretical premises, it provides only a modest step up in sensitivity

Short-term reproducibility of dipyridamole-echocardiography test.

The aim of this study was to assess the short-term reproducibility of dipyridamole-echocardiography test (DET) consisting of two-dimensional echo monitoring during dipyridamole infusion (up to 0.84 mg/kg in 10 min). The diagnostic end-point of the test is the detection of new onset or worsening regional asynergy. A group of 87 patients with rest and/or effort angina performed two DETS on two consecutive days. All 60 patients with a positive DET had a positive repeat test, and the 27 negative DETs were also negative on the following day. The timing of the asynergy was also very similar between the two tests, both in patients with angina on effort (r = .93, p less than 0.01) and at rest (r = .92, p less than 0.01). In conclusion, DET has a very high short-term reproducibility regarding the presence and timing of asynergy

Treatment of perinfarction recurrent ventricular fibrillation by percutaneous pharmacological block of left stellate ganglion

A patient suffering from an acute myocardial infarction presented on the seventh and eighth days of hospitalization recurrent episodes of ventricular fibrillation refractory to antiarrhythmic treatment. The life-threatening ventricular fibrillation was suppressed by percutaneous pharmacological block of the left stellate ganglion

Association Between Increased Mortality and Mild Thyroid Dysfunction in Cardiac Patients

BACKGROUND: The effects of subclinical thyroid dysfunction on cardiac outcome are not well defined. METHODS: To assess the relationship between mild thyroid dysfunction and the incidence of death in cardiac patients, we evaluated 3121 cardiac patients. Cardiac and overall deaths were considered. Four groups were defined: euthyroidism, subclinical hypothyroidism (SCH), subclinical hyperthyroidism (SCT), and low triiodothyronine syndrome (low T3). RESULTS: After mean follow-up of 32 months, there were 65 and 140 cardiac and overall deaths (3.4% and 7.3%), respectively, in euthyroidism, 15 and 27 (7.2% and 13.0%) in SCH, 8 and 9 (8.2% and 9.2%) in SCT, and 59 and 119 (6.5% and 13.1%) in low T3. Survival rates for cardiac death were lower in SCH, SCT, and low T3 than in euthyroidism (log-rank test; chi2 = 19.46; P < .001). Survival rates for overall death were lower in SCH and low T3 than in euthyroidism (log-rank test; chi2 = 26.67; P < .001). After adjustment for several risk factors, hazard ratios (HRs) for cardiac death were higher in SCH (HR, 2.40; 95% confidence interval [CI], 1.36-4.21; P = .02), SCT (HR, 2.32; 95% CI, 1.11-4.85; P = .02), and low T(3) (HR, 1.63; 95% CI, 1.14-2.33; P = .007) than in euthyroidism; HRs for overall death were higher in SCH (HR, 2.01; 95% CI, 1.33-3.04; P < .001) and low T3 (HR, 1.57; 95% CI, 1.22-2.01; P < .001) but not in SCT. CONCLUSION: A mildly altered thyroid status is associated with an increased risk of mortality in patients with cardiac disease

Acute Effects Of Triiodothyronine T. (T3) Replacement Therapy in Patients with Chronic Heart Failure and Low-T3 Syndrome: A Randomized, Placebo-Controlled Study

Context: Low-T3 syndrome is a predictor of poor outcome in patients with cardiac dysfunction. The study aimed to assess the short-term effects of synthetic L-T3 replacement therapy in patients with low-T3 syndrome and ischemic or nonischemic dilated cardiomyopathy (DC). Design:Atotal of 20 clinically stable patients with ischemic (n12) or nonischemic (n8) DC were enrolled. There were 10 patients (average age 72 yr, range 66–77; median, 25–75th percentile) who underwent 3-d synthetic L-T3 infusion (study group); the other 10 patients (average age 68 yr, range 64–71) underwent placebo infusion (control group). Clinical examination, electrocardiography, cardiac magnetic resonance, and bio-humoral profile (free thyroid hormones, TSH, plasma renin activity, aldosterone, noradrenaline, N-terminal-pro-B-Type natriuretic peptide, and IL-6) were assessed at baseline and after 3-d synthetic L-T3 (initial dose: 20 g/m2 body surfaced) or placebo infusion. Results: After T3 administration, free T3 concentrations increased until reaching a plateau at 24–48 h (3.43, 3.20–3.84 vs. 1.74, 1.62–1.93 pg/ml; P 0.03) without side effects. Heart rate decreased significantly after T3 infusion (63, 60–66 vs. 69, 60–76 beats per minute; P 0.008). Plasma noradrenaline (347; 270–740 vs. 717, 413–808 pg/ml; P 0.009), N-terminal pro-B-Type natriuretic peptide (3000, 438-4005 vs. 3940, 528-5628 pg/ml; P0.02), and aldosterone (175, 152–229 vs. 231, 154–324 pg/ml; P 0.047) significantly decreased after T3 administration. Neurohormonal profile did not change after placebo infusion in the control group. After synthetic L-T3 administration, left-ventricular end-diastolic volume (142, 132–161 vs. 133, 114–158 ml/m2 body surface; P 0.02) and stroke volume (40, 34–44 vs. 35, 28–39 ml/m2 body surface; P 0.01) increased, whereas external and intracardiac workload did not change. Conclusions: In DC patients, short-term synthetic L-T3 replacement therapy significantly improved neuroendocrine profile and ventricular performance. These data encourage further controlled trials with more patients and longer periods of synthetic L-T3 administration

Low-T3 Syndrome

Background— Clinical and experimental data have suggested a potential negative impact of low-T3 state on the prognosis of cardiac diseases. The aim of the present prospective study was to assess the role of thyroid hormones in the prognosis of patient population with heart disease. Methods and Results— A total of 573 consecutive cardiac patients underwent thyroid function profile evaluation. They were divided in two subgroups: group I, 173 patients with low T3, ie, with free T3 (fT3) <3.1 pmol/L, and group II, 400 patients with normal fT3 (≥3.1 pmol/L). We considered cumulative and cardiac death events. During the 1-year follow-up, there were 25 cumulative deaths in group I and 12 in group II (14.4% versus 3%, P <0.0001); cardiac deaths were 13 in group I and 6 in group II (7.5% versus 1.5%, P =0.0006). According to the Cox model, fT3 was the most important predictor of cumulative death (hazard ratio [HR] 3.582, P <0.0001), followed by dyslipidemia (HR 2.955, P =0.023), age (HR 1.051, P <0.005), and left ventricular ejection fraction (HR 1.037, P =0.006). At the logistic multivariate analysis, fT3 was the highest independent predictor of death (HR 0.395, P =0.003). A prevalence of low fT3 levels was found in patients with NYHA class III-IV illness compared with patients with NYHA class I-II (χ 2 5.65, P =0.019). Conclusions— Low-T3 syndrome is a strong predictor of death in cardiac patients and might be directly implicated in the poor prognosis of cardiac patients

Insulin resistance is a major determinant of myocardial blood flow impairment in anginal patients

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