Ilya Ovsyshcher

A simple bedside test of 1-minute heart rate variability during deep breathing as a prognostic index after myocardial infarction☆☆☆

BACKGROUND We evaluate a simple, bedside test that measures 1-minute heart rate variability in deep breathing as a predictor of death after myocardial infarction. METHODS Bedside heart rate variability was assessed in 185 consecutive patients 5.1 +/- 2.5 days after a first myocardial infarction. Patients were instructed to take 6 deep respirations in 1 minute while changes in heart rate were measured and calculated by an electrocardiographic recorder. An abnormal test result was defined as a difference of less than 10 beats/min between the shortest and longest heart rate interval. RESULTS Heart rate variability <10 beats/min was found in 65 patients (35%) and was significantly lower (P <.05) in women, patients >60 years of age, patients with diabetes, patients with congestive heart failure, and patients taking angiotensin-converting enzyme inhibitors. Mean follow-up period was 16 months. Ten patients died during follow-up: 9 of cardiac causes and 1 of stroke. Nine of these 10 patients had heart rate variability <10 beats/min (P =.004). The sensitivity and specificity of this test for cardiovascular mortality is 90.0% and 68.0%, respectively. The negative predictive value is 99.2% and the relative risk is 16.6. Heart rate variability <10 beats/min remained a significant predictor of death after adjusting for clinical, demographic, and left ventricular function with an odds ratio of 1.38 (95% confidence interval, 1.13-1.63). CONCLUSIONS This simple, brief bedside deep breathing test of heart rate variability in patients after myocardial infarction appears to be a good predictor for all-cause mortality and sudden death. It may be used as a clinical test for risk stratification after myocardial infarction.

Measurements of cardiac output by impedance cardiography in pacemaker patients at rest: Effects of various atrioventricular delays

OBJECTIVES The purpose of this study was to evaluate the ability of impedance cardiography to determine the change in cardiac output caused by modifications in the atrioventricular (AV) delay in DDD (dual-chamber) pacing mode while pacing the atrium and ventricle at different programmed rates. BACKGROUND Impedance cardiography permits continuous noninvasive monitoring of hemodynamic variables on a beat to beat basis. METHODS Eleven patients with a DDD pacemaker were evaluated by impedance cardiography. Stroke volume, cardiac output and total peripheral resistance were assessed in the supine rest position during both DDD and ventricular (VVI) pacing. Hemodynamic variables were measured during DDD pacing at rates ranging from 60 to 110 beats/min in 10-beats/min increments with programmed AV delay varying from 50 to 250 ms in 50-ms increments. When the pacemaker was reprogrammed to the VVI pacing mode, these measurements were repeated at the same pacing rates. RESULTS Cardiac output measurements during programmed conditions were found to be highly reproducible. The mean coefficient of variation was 3% during DDD pacing; it was 6% in the VVI pacing mode. A large decrease in cardiac output (approximately 30%) was found when a pacemaker was reprogrammed from the DDD to the VVI pacing mode. At DDD pacing rates between 70 to 110 beats/min, the highest cardiac output occurred at an average AV delay of < 120 ms from atrial stimulus to ventricular stimulus. At an average AV delay of > or = 200 ms, the cardiac output in the DDD and VVI pacing modes was similar. CONCLUSIONS 1) Impedance cardiography allows highly reproducible noninvasive assessments of cardiac output in pacemaker patients; 2) inappropriate programming of the AV interval in patients with atrial and ventricular pacing can decrease cardiac output significantly, and the extent of the decrease is similar to or less than that observed in ventricular pacing; 3) hemodynamic measurements obtained with impedance cardiography can facilitate optimal programming of pacemaker variables.

Right Atrial Thrombus and Recurrent Pulmonary Emboli Secondary to Permanent Cardiac Pacing—A Case Report and Short Review of Literature

A patient with a right atrial thrombus and recurrent pulmonary emboli sec ondary to permanent pacemaker insertion is described. Possible precipitating factors were damage to the subclavian vein, congestive heart failure, paroxys mal atrial fibrillation, and immobilization. Venography demonstrated a large atrial thrombus in the superior vena cava and right atrium. The patient was successfully treated with heparin and subsequently with warfarin and dipyrida mole.

Left ventricular performance in patients with atrial septal defect: evaluation with noninvasive methods.

Eighteen patients with an atrial septal defect (Group I) and 45 patients whose defect had been repaired (Group II) were studied with echocardiography and systolic time Intervals. All patients In Group I had an increased right ventricular diameter (mean 24.5 mm/m2) that showed a direct linear relation to the size of the shunt (Qp/Qs ratio). In Group II the right ventricular diameter was significantly smaller (mean 15.6 mm/m2) (P < 0.001). The left ventricular diameter measured less than the mean normal value in 13 of the 18 patients in Group I (mean 23.2 mm/m2) and was significantly larger in the 45 in Group II (mean 27.7 mm/m2) (P < 0.001). Comparison of systolic time intervals in Groups I and II showed that patients in the former group had shorter mean left ventricular ejection time index (LVETI) (407.9 versus 420.8 msec, P < 0.05), a longer mean preejection period index (PEPI) (140.9 versus 126.7 msec, P < 0.001) and a higher mean ratio of preejection period to ejection time (PEP/LVET) (0.39 versus 0.33, P < 0.001). A direct linear relation existed between both the preejection period index and the PEP/LVET ratio and the size of the shunt (Qp/Qs) in Group I. In three patients the abnormal systolic time intervals were consistent with mildly diminished left ventricular performance preoperatively but promptly returned to normal postoperatively. However, echocardiographic assessment revealed that left ventricular wall contractility was normal or hyperdynamic in all cases. The mildly diminished overall left ventricular performance as shown by systolic time intervals appears to be related to the volume overload of the right ventricle and to the concomitantly diminished volume of the left ventricle rather than to any impairment of myocardial contractility. After closure of the defect the size of the ventricle and its performance return to normal.

Evaluation of a new rate adaptive ventricular pacemaker controlled by double sensors

The LEGEND‐PLUS, a new rate adaptive pacemaker that combines activity and minute ventilation sensing for automatic rate adaptation was implanted in the right ventricle (VVIR) in 11 patients (mean age 62 ± 9 years). Initial programming was performed using the Programmer Exercise Protocol (a 3‐minute walk). This programming was evaluated by treadmill tests, up‐stairs and down‐stairs walking, and Holier recordings. Results: Following the final programming of LEGEND‐PLUS, the mean upper activity rate was 102 ± 7 beats/rain (range 90–120 beats/min), while the mean upper minute ventilation rate was 125 ± 16 beats/min (range 100–150 beats/min). The mean rate responses during the exercise protocol and the final programming in minute ventilation and activity sensing modes were 5.4 ± 2.3 (range 1–9), versus 4 ± 2.4 (range 1–8; P < 0.01) and 7.6 ±1.1 (range 5–9), versus 7.5 ± 0.8 (range 6–9; P = 0.8), respectively. In the combined sensing mode, the acceleration rate was identical to the activity rate response and the deceleration rate mimicked the minute ventilation. Conclusion: Dual sensor VVIR pacemakers have the potential to improve rate adaptation to exercise. The rate response to exercise in patients fitted with activity and minute ventilation sensors, VVIR pacemakers closely mimics the physiological rate response.

Concomittant ST elevation in inferior and anterior leads in acute myocardial infarction: Clinical and Anatomical Significance

Various instances of acute myocardial infarction that may cause concomittant ST-segment elevation in inferior and anterior leads are presented. Among the situations that produce this phenomenon are: (1) multivessel coronary artery disease or isolated disease of a dominant left anterior descending artery causing combined inferior and anterior myocardial infarction; and (2) isolated disease of a right coronary artery causing combined infarction, or isolated right ventricular myocardial infarction. The mechanisms responsible for the electrocardiographic patterns in each instance are discussed.

ST Elevation in Leads V1 to V4 Caused by Isolated Right Ventricular Ischemia and Infarction

A patient with isolated right ventricular ischemia and infarction is presented. ST elevation in leads V1 to V4 mimicking anteroseptal myocardial infarction was recorded at admission and during episodes of chest pain later on. Noninvasive and invasive workup suggested isolated right ventricular infarction and ischemia due to an occluded small and nondominant right coronary artery.

Atypical ventricular tachycardia and alternating Osborn waves induced by spontaneous mild hypothermia

SummaryA one-month-old infant developed atypical ventricular tachycardia, complete right bundle branch black, and alternating 2:1 Osborn waves during spontaneous mild hypothermia; 10 h after rewarming, the electrocardiogram was normal.

Transient complete atrioventricular block induced by a chest thump in a patient with ventricular tachycardia

We describe an unusual case of transient complete atrioventricular block induced by a chest thump during resuscitation in a patient with ventricular tachycardia.

Short- and Long-Term Comparative Study of Anistreplase Versus Streptokinase in Acute Myocardial Infarction

Streptokinase is well established as an effective thrombolytic. Anistreplase, a new thrombolytic drug, is a complex of streptokinase and acylated human plas minogen that can be administered by intravenous bolus and activates plasmino gen at the clot site. Although both streptokinase and anistreplase are effected in treating myocardial infarction (MI), they have different pharmacologic proper ties. This study was designed to identify short- and long-term differences in their clinical effectiveness, safety in use, and survival rates in patients with acute MI. One hundred ten successive patients under seventy years of age admitted within three hours after onset of sustained chest pain suggestive of acute MI were randomized to receive either 30 units of anistreplase intravenously over five minutes or intravenous injection of 750,000 units of streptokinase over thirty to sixty minutes. Reperfusion was achieved in 34 of the 52 (65%) patients treated with anis treplase and in 41 of the 58 (71%) patients treated with streptokinase (p = NS). The two drugs were equally effective in preserving left ventricular ejection frac tion, which was found to be significantly better in patients with anterior wall MI who had achieved reperfusion than it was in those who did not (p < 0.02). One-month, twelve-month, and thirty-six-month survival rates were high (96% to 88%) with no significant difference between the two treatment groups. The authors conclude that the two drugs are equally effective thrombolytic agents but that anistreplase has the advantage that it can be administered as a bolus injection.