Hemodynamic effects of new intra-aortic balloon counterpulsation timing methods in patients: a multicenter evaluation.

BACKGROUND: To test whether later intra-aortic balloon pump (IABP) deflation approaching or simultaneous with left ventricular ejection would improve hemodynamics and myocardial efficiency with the use of new balloon deflation methods, 4 IABP timing techniques were evaluated in 43 patients. METHODS AND RESULTS: Later balloon deflation produced significantly greater percentage changes in mean aortic pressure (6% vs 1%), systolic pressure time index (-27% vs -20%), diastolic pressure time index (35% vs 19%), and the systolic pressure-time index/diastolic pressure-time index ratio (97% vs 51%), respectively. However, these changes increased peak systolic pressure (-15% vs -11%). Cardiac output and stroke volume indexes were not significantly altered over the 4 settings. CONCLUSIONS: These data suggest that systemic hemodynamics and myocardial efficiency may be improved by later balloon deflation approaching left ventricular ejection in comparison to conventional IABP timing.

Dendritic nucleic acid structures.

Dendritic molecules are highly-branched arborescent structures and have found applications as chemical reagents, lubricants, contrast media for magnetic resonance, and others. Dendritic nucleic acids could be extremely useful for the development of nucleic acid diagnostics as signal amplification tools and potentially as drug (antisense) delivery vehicles. Further, due to the relatively large size of nucleic acid molecules, nucleic acid dendrimers could be readily labeled with numerous fluorescent compounds and/or protein moieties with limited steric hindrance and/or quenching. Herein, we present a physical-mathematical model of a new class of dendrimers, constructed entirely from unique nucleic acid monomers that are designed such that sequential hybridization adds successive layers of monomer in a geometric expansion of both mass and free single-stranded sequences, called arms, at the surface. The specially designed monomer is a heterodimer of two single-stranded nucleic acid oligomers possessing a central double-stranded waist and four single-stranded arms for binding. Assembly of a dendrimer is initiated from a single monomer and proceeds in layers, the first comprising four monomers, which provides 12 single-stranded arms. Thus, the second layer adds 12 monomers resulting in 36 single-stranded arms. After addition of the 6th layer, the dendrimer is comprised of 1457 monomers, of which 972 reside in the 6th layer, which possesses 2916 single-stranded arms. The accompanying mathematical description of a dendrimer's growth is generic. A natural consequence and limiting condition of the growth process we describe is a saturated solution of nucleic acid, which is, in effect, a "nucleic acid membrane".

Determinants of defibrillation: prospective analysis of 183 patients.

Previous studies have suggested that a number of factors may influence the ability to defibrillate: the transthoracic resistance and resultant current flow, the paddle electrode size, the duration of preshock ventricular fibrillation (VF) and cardiopulmonary resuscitation, metabolic abnormalities, body weight, the shock energy selected, and whether the patient is receiving lidocaine. To examine the effect of these variables, a prospective study was conducted of 183 patients who received direct-current shocks for VF. Overall defibrillation rates approached 90%, even in patients with secondary VF, but rates of successful resuscitation and survival were much lower. Patients who never defibrillated despite multiple shocks had a prolonged duration of cardiopulmonary resuscitation preceding the first shock (21 +/- 14 minutes) and systemic hypoxia and acidosis. These conditions tended to occur in patients who initially had cardiac arrest from causes other than VF: asystole, severe bradycardia and electromechanical dissociation. In such patients, VF developed only as a late event, which was then often unresponsive to attempted defibrillation. The other factors examined were not major determinants of defibrillation.

Effect of ischemia, hypertrophy, hypoxia, acidosis, and alkalosis on canine defibrillation.

Our purpose was to assess the effect of myocardial ischemia, left ventricular hypertrophy, and systemic hypoxia and acid-base abnormalities on the energy requirements for defibrillation. We determined the defibrillation threshold (DFT), the minimum energy required to defibrillate. DFT was not significantly elevated after left anterior descending coronary occlusion, nor was there a relationship between the size of the occluded coronary distribution area (coronary risk area) and the change in DFT in individual animals. Renal hypertension and left ventricular hypertrophy were induced by unilateral nephrectomy and contralateral renal artery stenosis. DFT in left ventricular hypertrophy dogs was not significantly higher than in dogs without hypertrophy. Finally, we induced systemic hypoxia and acid-base abnormalities. Neither respiratory nor metabolic acid-base disturbances affected DFT, but during systemic hypoxia (O2 tension 45 +/- 2) DFT fell from 83 +/- 49 to 58 +/- 28 J (P less than 0.01). Thus in dogs, myocardial ischemia, left ventricular hypertrophy, and acid-base abnormalities do not elevate defibrillation energy requirements, whereas hypoxia reduces the energy needed to defibrillate.

Clinical evaluation of the Percor percutaneous intraaortic balloon: cooperative study of 722 cases.

Clinical experience with the Percor percutaneous intraaortic balloon (IAB) was reviewed in 722 cases performed by 59 clinicians (35 surgeons and 24 cardiologists). Compared with standard IABs, Percor was judged to provide easier insertion by 88% of clinicians, easier femoral-iliac passage by 29%, easier aortic passage by 36%, and easier final positioning by 19%; the Percor IAB was rated more difficult in these respects by 2-5% of users; the rest of the responders found no significant difference in these measures. Technical problems included an inability to negotiate sclerotic vessels in 12.6%, delayed hemostasis in 1.9%, and the need for surgical repair of the arteriotomy site in 2%. Medical complications included peripheral ischemia in 5.3%, emboli in 3.6%, arterial dissection in 1.9%, dislodged arterial plaque in 1.1%, perforation of the arterial tree in 1.0%, local femoral thrombosis in 1.0%, and poor intraoperative hemostasis in 0.3%. Local wound infection, ischemic amputation or neuropathic sequelae were not reported. Mechanical counterpulsation with Pecor was equivalent to that of standard IABs, but by subjective judgments, 80% rated Percor more desirable and 47% safer; 3% rated it less desirable and 10% less safe. With Percor, earlier clinical use of IAB pumping was seen by 73%, and new or additional indications were recommended by 19%.

Elective cardioversion: influence of paddle-electrode location and size on success rates and energy requirements.

We compared the success rates and energy requirements of two electrode-paddle positions (anteroposterior vs. anterolateral) and different paddle sizes in the elective cardioversion of atrial arrhythmias. We prospectively studied 173 patients - 111 in atrial fibrillation and 62 in atrial flutter. The anterolateral paddles used were either two standard-size (8.5-cm diameter) paddles or one 13-cm diameter anterior paddle with one standard-size lateral paddle. The anteroposterior paddles used were either a standard-size or a 13-cm anterior paddle with 12-cm posterior paddle. Overall cardioversion success rates with either paddle position were similar (greater than 90 per cent). The larger paddles did not significantly reduce energy requirements for cardioversion of either arrhythmia. We conclude that anterolateral paddles are as effective as anteroposterior paddles for the elective cardioversion of atrial arrhythmias, and that there is no demonstrable advantage to using paddles that are larger than the standard size in either position.

Transthoracic resistance in human defibrillation. Influence of body weight, chest size, serial shocks, paddle size and paddle contact pressure.

Successful defibrillation depends on delivery of adequate electrical current to the heart; one of the major determinants of current flow is transthoracic resistance (TTR). To study the factors influencing TTR, we prospectively collected data from 44 patients undergoing emergency defibrillation. Shocks of 94-450 J delivered energy were administered from specially calibrated Datascope defibrillators that displayed peak current flow, thereby permitting determination of TTR. Shocks were applied from standard (8.5-cm diameter) or large (13 cm) paddles placed anteriorly and laterally. First-shock TTR ranged from 15-143 omega. There was a weak correlation between TTR and body weight (r = 0.45, p less than 0.05) and a stronger correlation between TTR and chest width (r = 0.80, p less than 0.01). Twenty-three patients who were defibrillated using standard 8.5-cm paddles had a mean TTR of 67 +/- 36 omega (+/- SD), whereas 21 patients who received shocks using paddle pairs with at least one large (13 cm) paddle had a 21% lower TTR of 53 +/- 24 omega (p = 0.05, unpaired t test). Ten patients received first and second shocks at the same energy level; TTR declined only 8%, from 52 +/- 19 to 48 +/- 16 omega (p less than 0.01, paired t test). In closed chest dogs, shocks were administered using a spring apparatus that regulated paddle contact pressure against the thorax. Firmer contact pressure caused TTR to decrease 25%, from 48 +/- 22 to 36 +/- 17 omega (p less than 0.01, paired t test). Thus, human TTR varies widely and is related most closely to chest size. TTR declines only slightly with a second shock at the same energy level. More substantial reductions in TTR and declines only slightly with a second shock at the same energy level. More substantial reductions in TTR and increases in current flow can be achieved by using large paddles and applying firm paddle contact pressure.

Effect of direct-current countershocks on regional myocardial contractility and perfusion. Experimental studies.

Very high energy electrical countershocks can cause morphologic damage to the myocardium. In this study we searched for functional correlates of these shock-induced morphologic changes. We used ultrasonic sonomicrometers to measure myocardial contractility and radiolabeled microspheres to assess perfusion. Acute and chronic experiments were conducted in 45 dogs, assessing the effect of both direct (epicardial) and transthoracic shocks on beating and fibrillating hearts. High-energy or rapidly repeated epicardial shocks caused subepicardial contraction abnormalities. This indicates that electrical current delivered to the myocardium in sufficiently high amounts and concentration can cause functional damage. Thus, in open-chest defibrillation during cardiac surgery, low energies (10-20 J) should be used initially and higher energies resorted to only if lower-energy shocks fail. However, single and multiple transthoracic shocks up to 460 J delivered energy caused no detectable contraction abnormalities. Myocardial perfusion did not fall after shocks. Thus, high-energy transthoracic shocks may have no deleterious effects on the contraction and perfusion of normal myocardium.

Left-axis deviation: etiologic factors in one-hundred patients.

Clinical and electrocardiographic findings were analyzed in 100 consecutive cases of LAD. Below the age of forty years, LAD was uncommon, but its incidence increased continuously thereafter. The most frequent primary clinical diagnosis was arteriosclerotic heart disease. The functional mechanism producing LAD most often was LAHB, responsible in about 40 per cent. Approximately half the instances of LAHB were associated with old myocardial infarction of septal, anterior, or lateral regions, but half were seen in the absence of infarction or clinical coronary sclerosis and are presumed due to primary degenerative processes within these specialized conducting fibers. Approximately one-sixth of the instances of LAD were due to loss of inferior forces following inferior myocardial infarction. Typical left ventricular hypertrophy was a distinctly uncommon cause of LAD. Last, in 24 patients with LAD the mechanism or cause was not evident initially, of which two were subsequently shown to represent a very mild degree of LAHB. Also it is suggested that asymmetric myocardial hypertrophy of the anterior wall may account for some instances of LAD not otherwise explained.