Atrial premature complexes and heart rate have prognostic significance in 1-month atrial fibrillation recurrence after electrical cardioversion.

AIMS: The aim of this study was to investigate the significance of simple 24-h Holter (24H) data after electrical cardioversion (CV) for atrial fibrillation (AF) recurrence. METHODS: We prospectively studied 47 consecutive patients subjected to CV, who successfully converted to sinus rhythm. All underwent echocardiography and 24H after CV. AF recurrence was studied at 14 days and 1 month by second 24H or by interim report of AF. RESULTS: About 53.2% remained in sinus rhythm (group I) and the rest recurred to AF (group II). Group I had fewer atrial premature complexes per hour (APC/h) (P = 0.002) and lower maximum (max HR), average, and minimum heart rates compared with group II (all Ps < 0.05). The optimal value of APC/h and max HR with best sensitivity and specificity was 32 APC/h and 90 bpm, respectively. These findings were the predictors of AF recurrence [hazard ratio (HR) = 4.5 with 95% CI = 1.7-11.7 and HR = 4.3 with 95% CI = 1.7-10.9, respectively]. Patients with the combination of both predictors had greater HR of AF recurrence compared with those with < 32 APC/h and max HR < 90 bpm (HR = 8.8 with 95% CI = 2.5-31.4). CONCLUSION: Patients with frequent APC/h and high max HR are at high risk for 1-month AF recurrence after electrical CV.     

Peripheral levels of matrix metalloproteinase-9, interleukin-6, and C-reactive protein are elevated in patients with acute coronary syndromes: correlations with serum troponin I

BACKGROUND: Acute coronary syndromes (ACS) are characterized by activation of systemic and local inflammatory mediators. The interrelation between these soluble inflammatory markers and their association with markers of myocardial necrosis have not been extensively studied. HYPOTHESIS: The study was undertaken to evaluate the association of the systemic levels of matrix metalloproteinase-9 (MMP-9) and the tissue inhibitor of metalloproteinase-1 (TIMP-1), with C-reactive protein (CRP), interleukin-6 (IL-6), and serum troponin-I in patients admitted with ACS. METHODS: Analysis of serum concentrations of the above inflammatory markers was performed in 53 patients with unstable angina (UA) and in 15 with non-ST-segment elevation myocardial infarction (NSTEMI) within 48 h of admission, and 34 patients with stable coronary artery disease. RESULTS: Compared with patients with stable angina, those with ACS had elevated admission levels of MMP-9 (p = 0.04), CRP (p < 0.001), and IL-6 (p = 0.001), but not TIMP-1 (p = 0.55). Compared with patients with UA, those with NSTEMI also had higher levels of IL-6 (p < 0.001), CRP (p = 0.002), and MMP-9 (p = 0.05). CONCLUSIONS: In patients with ACS, the admission levels of inflammatory mediators, including MMP-9, CRP, and IL-6 are significantly elevated, specifically in association with serum troponin I. Systemic and local markers of inflammatory activity may be directly associated with myocardial injury.     

Effect of digitalis on diminished baroreceptor sensitivity in diabetics.

The baroreceptor sensitivity was estimated in 50 normal controls (Group A) and in 50 diabetics of comparable age (Group B). The technique used was infusion of angiotensin (0.5 microgram/min) and measurement of the bradycardic response resulting from the increase of blood pressure. The slope was used as an index of baroreceptor sensitivity. Diabetics had significantly lower baroreceptor sensitivity and a higher resting heart rate. Sensitivity decreased with age in both groups. The reproducibility of the method was excellent. Deslanoside-C (0.8 mg) significantly increased the baroreceptor sensitivity in 11 normal controls and 9 diabetics. Very low sensitivity was found in 26 diabetics who had no evidence of orthostatic hypotension, neuropathy, or retinopathy. However all 17 patients with the above findings had very low sensitivity.     

Diastolic coronary artery narrowing due to left ventricular dilatation

A 56 year old man with a large anterior myocardial infarction and diffuse left ventricular hypocontractility and dilatation was found to have narrowing of the distal part of the left anterior descending coronary artery in diastole. This most unusual finding was ascribed to diastolic compression of the vessel by the enlarged left ventricle. Only 3 similar cases have been found in the literature up to now.     

Deoxycytidylate deaminase in the diagnosis of acute myocardial infarction

The diagnostic value of deoxycytidylate deaminase (dCMP) in the diagnosis of acute myocardial infarction (AMI) was examined in 31 healthy controls and 32 patients with proven AMI. Its specificity in normal controls was 93.5%. Its highest levels were measured on the 3rd to 5th post-infarct day, when its sensitivity reached 97.5%. Its diagnostic performance was similar to that of SGOT, total LDH1/LDH2 ratio greater than 1, total CPK and CPK-MB. Its peak levels showed a highly significant correlation (p less than 0.001) with those of the above enzymes. The measurement of dCMP may be a valuable complement in the diagnosis of AMI since this enzyme is not affected by lung infarction or hemolysis. Moreover, since it expresses tissue regeneration rather than destruction it may aid in the assessment of various interventions designed for the promotion of myocardial healing process.     

Dissection During Restenotic Lesion Balloon Angioplasty: Comparison with Initial Angioplasty

The aim of this study was to assess the frequency and severity of dissection during repeat angioplasty for restenosis, to correlate the occurrence of this event with the lesion characteristics and the procedure-related factors and to examine if dissection during initial angioplasty predisposes to dissection during the repeat procedure. Sixty-nine significant lesions in native coronary arteries were treated with balloon angioplasty (A?PTCA) and retreated for restenosis with balloon angioplasty (B?PTCA). Dissection was detected less frequently during B?PTCA (7/69 vs. 18/69, p < 0.05). Anatomic variables did not differ significantly between A? and B?PTCA. Balloon to artery ratio (B/A ratio) was slightly but significantly higher during B?PTCA (1.03 +/- 0.13 vs. 0.97 +/- 0.14, p < 0.05) and duration of inflation was shorter (377 +/- 218 vs. 473 +/- 305 sec, p < 0.05). In 17 out of the 18 lesions which were dissected during A?PTCA, dissection did not occur during B?PTCA, despite the application of a higher B/A ratio (1.05 +/- 0.13 vs. 0.97 +/- 0.17, p < 0.05). Duration of inflation was shorter during B?PTCA (390 +/- 227 vs. 639 +/- 394 sec, p < 0.05). Six out of seven lesions which were dissected during B?PTCA had not been dissected during A?PTCA. In this subgroup, lesion characteristics did not differ between the two interventions and duration of inflation was shorter during B?PTCA (340 +/- 101 vs. 458 +/- 128, p < 0.05). CONCLUSIONS: Dissection occurred less frequently during restenotic lesion PTCA. Dissection during A?PTCA did not predispose to dissection during B?PTCA. These findings may be ascribed to the proliferative nature of the restenotic process.     

Loss of cardioprotection induced by ischemic preconditioning after an initial ischemic period in isolated rat hearts

BACKGROUND:

The beneficial effect of ischemic preconditioning (PC) has been extensively studied in normal hearts but its effects on diseased hearts remain largely unknown. The effect of PC in the already ischemic myocardium has not been previously studied, although ischemia in varying intervals, which is difficult to assess, is often encountered in clinical practice.

OBJECTIVE:

To investigate whether the cardioprotective effect of PC is preserved when it is applied after a period of ischemia of varying duration.

METHODS:

Male Wistar rats were used for this study. Isolated normal rat hearts were perfused in Langendorff mode. Before 20 min of zero flow global ischemia followed by 45 min of reperfusion, hearts were subjected to an initial 20-min period of ischemia followed by 10 min of reperfusion (group A1); an initial 20-min period of ischemia followed by 10 min of reperfusion and two-cycle PC (3 min of ischemia, 5 min of reperfusion followed by 5 min of ischemia and 5 min of reperfusion) (group A2); and two-cycle PC followed by the initial 20-min period of ischemia and 10 min of reperfusion (group A3).Groups B and C were subjected to an initial ischemia of 15 min and 10 min, respectively, and subgroups 1, 2 and 3 were treated as above. Left ventricular end-diastolic pressure was measured at 45 min of reperfusion (LVEDP45 in mmHg). Postischemic recovery of left ventricular developed pressure was expressed as a percentage of the initial value (LVDP%).

RESULTS:

LVDP% and LVEDP45 were similar between groups A1 and A2, while when ischemic preconditioning preceded the two periods of ischemia (group A3), it resulted in significantly higher LVDP% and significantly lower LVEDP45 compared with groups A1 and A2. Left ventricular functional recovery was not increased in group B2 compared with group B1. LVDP% and LVEDP45 were similar among groups C1, C2 and C3.

CONCLUSION:

Ischemic preconditioning does not improve functional recovery in isolated rat hearts that have been initially subjected to 20 min or 15 min of zero-flow global ischemia, while an initial 10-min ischemic period seems to precondition the heart.