Primary angioplasty for acute myocardial infarction in octogenarians.
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Age Factors↗
Biomedical subjects
M Noc
Publications and source records attributed to M Noc.
Double vessel extension of spontaneous left main coronary artery dissection in young women treated with thrombolytics.
Spontaneous coronary artery dissection is an extremely rare cause of myocardial infarction. The prognosis and treatment of coronary artery dissection have not yet been defined. We report on a 42-year-old woman who was admitted to the emergency unit of a regional hospital with central chest pain and electrocardiographic signs of extensive acute anterior myocardial infarction (MI). She was treated with thrombolytics, yet her condition deteriorated rapidly, resulting in cardiogenic shock. An angiogram revealed dissection of the left main coronary artery that extended into the anterior descending (LAD) and circumflex arteries (LCX). At autopsy a recent anterolateral MI of the left ventricle was found. Dissection of the left coronary artery system was confirmed. Extension of the dissection may have been due to thrombolytic treatment.
Adult↗
Elevated troponin I level on admission is associated with adverse outcome of primary angioplasty in acute myocardial infarction.
BACKGROUND: In patients with acute myocardial infarction (AMI) undergoing thrombolytic therapy, an elevated troponin level on admission is associated with a lower reperfusion rate and a complicated clinical course. Whether an elevated troponin level on admission similarly predicts an adverse outcome in patients undergoing primary angioplasty is currently unknown and was investigated in the present study. METHODS AND RESULTS: Cardiac troponin I (cTnI) was determined on admission in 110 consecutive patients with AMI associated with ST-segment elevation or left bundle branch block who underwent primary angioplasty. Fifty-four patients (49%) had an elevated cTnI (>/=0.4 ng/mL) on admission. In patients with elevated cTnI, primary angioplasty was less likely to achieve TIMI 3 flow (as classified by the Thrombolysis in Myocardial Infarction trial) in univariate (76% versus 96%, P:=0.03) or in multivariate (odds ratio 0.1, 95% CI 0.02 to 0.54) analysis. Patients with elevated cTnI were more likely to develop congestive heart failure (23% versus 9%, P:<0.05) and death, heart failure, or shock (30% versus 9%, P:=0.006). Elevated cTnI remained a significant predictor of the composite end point after controlling for other clinical data that were available early in the course, including time to presentation and angiographic results (relative risk 5.2, 95% CI 1.03 to 26.3). During a follow-up of 426+/-50 days, elevated admission cTnI was a predictor of cardiac mortality (11% versus 0%, P:=0.012), adverse cardiac events (cardiac mortality or nonfatal reinfarction; 19% versus 5.4%, P:=0.04), and adverse cardiac events plus target vessel revascularization (32% versus 14%, P:=0.054). CONCLUSIONS: In patients with ST-segment elevation AMI, an elevated cTnI on admission is associated with an increased risk of primary angioplasty failure and a more complicated clinical course.
Acute Disease↗
Acute isoniazid neurotoxicity during preventive therapy.
OBJECTIVE: To describe rare side effects of treatment with isoniazid. DESIGN: Descriptive case report. SETTING: Medical intensive care unit in a university medical center. PATIENT: A 14-yr old previously healthy girl receiving preventive isoniazid therapy who suddenly developed generalized tonic-clonic seizures and coma. INTERVENTIONS: Patient was sedated and mechanically ventilated. She also received pyridoxine intravenously. MEASUREMENTS AND MAIN RESULTS: An isoniazid overdose was not confirmed. Computed tomography of the brain and electroencephalogram revealed nothing abnormal. Seizures gradually disappeared within 2 hrs after sedation and treatment with pyridoxine. The patient was discharged on day 14 without consequences and has been well for 10 mos. No seizures reappeared after isoniazid was discontinued. CONCLUSIONS: We caution against possible isoniazid neurotoxicity in healthy individuals using recommended preventive doses.
Acute Disease↗
Electrocardiographic prediction of the success of cardiac resuscitation.
OBJECTIVES: To identify a method for predicting the success or failure of a defibrillatory shock such as to avoid potentially detrimental interruptions of cardiopulmonary resuscitation (CPR). Such a method would also guide more optimal programming of automated external defibrillators. DESIGN: Prospective, observational animal study. SETTING: Medical research laboratory in a university-affiliated research and educational foundation. SUBJECTS: Domestic pigs. INTERVENTIONS: Ventricular fibrillation (VF) was electrically induced in 66 domestic pigs. After an interval of between 3 and 5 mins of untreated VF, precordial compression was begun. Electrocardiographic lead 2 was monitored and artifacts produced during precordial compression were removed by digital filtering. MEASUREMENTS AND MAIN RESULTS: In the derivation study, electrical defibrillation restored spontaneous circulation in 30 of the 66 animals. Successfully resuscitated animals had significantly greater coronary perfusion pressure, maximum VF amplitude, mean VF amplitude, and dominant VF frequency. No animals were resuscitated if the coronary perfusion pressure was <8 mm Hg, maximum amplitude was <0.48 mV, mean amplitude was <0.25 mV, or dominant frequency <9.9 Hz independently of the duration of untreated VF. When mean amplitude and dominant frequency were combined, the predictability was further improved. In an additional validation study of 14 animals, consecutive defibrillations were uniformly unsuccessful if the combination of mean amplitude and dominant frequency did not exceed the threshold values obtained in derivation study. CONCLUSION: Mean VF amplitude alone or in combination with dominant frequency of VF was expressed as a numerical score. It served as an objective noninvasive measurement on a par with that of coronary perfusion pressure for predicting the success of defibrillation. As such, it minimizes the detriment of repetitively interrupting mechanical interventions during CPR for electrical defibrillation when an electrical shock predictably fails to restore an effective rhythm.
Animals↗
Acute myocardial infarction-failed thrombolysis followed by severe upper gastrointestinal bleeding.
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Aspirin↗
Profound circulatory shock following heroin overdose.
A 17-year-old previously healthy girl with profound circulatory shock following a heroin overdose is reported. Except for opiates no other substances and specifically no cocaine were found in the blood and urine samples. Even though the mechanism of shock is not completely understood, severe depression of left ventricular contractility seems to be the predominant reason. Acute right heart failure with decreased pulmonary capillary wedge pressure and arterial vasodilatation resulting in maldistribution of cardiac output cannot be ruled out as possible contributing factors. The shock was successfully reversed with volume loading and a high dose of dobutamine. The recovery was uneventful and the patient was discharged with normal cardiac function.
Adolescent↗
Treatment of out-of-hospital cardiac arrest in Ljubljana: outcome report according to the 'Utstein' style.
We investigated survival of patients with out-of-hospital cardiac arrest in Ljubljana according to the 'Utstein' style. Ljubljana consists of urban, suburban and semi-rural communities which encompass an area of 1615 km2 with 397306 residents. The area is served by a single response emergency medical system and local family practitioners. Between January 1, 1995 and December 31, 1997 cardiac arrest was confirmed in 966 patients. Cardiopulmonary resuscitation was attempted in 454 patients (47%). Collapse of presumed cardiac etiology (337 patients) was either bystander-witnessed (89%), un-witnessed (9%) or EMS personnel-witnessed (2%). Asystole was documented in 55%, ventricular fibrillation or tachycardia in 36% and other non-perfusing rhythms in 9% of these patients. Lay-bystander basic life support was performed in 19%. Nineteen patients (5.6%) survived to hospital discharge and 12 of them were independent in daily life. The survival of subgroups with bystanders-witnessed collapse and bystanders-witnessed ventricular fibrillation was 6.4 and 13%, respectively. Collapse of non-cardiac etiology (117 patients) was preceded by either respiratory failure (41), politrauma (22), circulatory shock (19), cerebrovascular incident (ten), intoxication (nine), strangulation (seven), electrocution (five) or drowning (four patients). Only five patients (4.2%) survived to hospital discharge. Hospital treatment of patients after successful initial cardiopulmonary resuscitation was associated with high mortality and required considerable resources.
Activities of Daily Living↗
Diagnosis and treatment of shock due to massive pulmonary embolism: approach with transesophageal echocardiography and intrapulmonary thrombolysis.
STUDY OBJECTIVES: To evaluate the diagnostic value of transesophageal echocardiography (TEE) as an initial diagnostic tool in shocked patients. The second objective was to study therapeutic impact of intrapulmonary thrombolysis in patients with diagnosed massive pulmonary embolism. DESIGN: Prospective observational study. SETTING: Medical ICU in 800-bed general hospital. PATIENTS: Twenty-four consecutive patients with unexplained shock and distended jugular veins. MEASUREMENTS AND MAIN RESULTS: In 18 patients, right ventricular dilatation with global or segmental hypokinesis was documented. In addition, central pulmonary thromboemboli (12 patients), reduced contrast flow in right pulmonary artery (one patient), and right ventricular free wall akinesis (one patient) were found. No additional echocardiographic findings were apparent in four patients. According to pulmonary scintigraphy or autopsy, sensitivity of TEE for diagnosis of massive pulmonary embolism (MPE) in patients with right ventricular dilatation was 92% and specificity was 100%. In patients without right ventricular dilatation, left ventricular dysfunction (four patients) or cardiac tamponade (two patients) was confirmed. Intrapulmonary thrombolysis was evaluated in 11 of 13 patients with MPE. Two patients died prior to attempted thrombolysis. Three patients received streptokinase and eight received urokinase. Twenty-four hours after beginning of treatment, total pulmonary resistance index significantly decreased for 59% and mean pulmonary artery pressure for 31%. Cardiac index increased for 74%. Nine of 11 patients receiving thrombolysis survived to hospital discharge. CONCLUSION: Bedside TEE is a valuable tool for diagnosis of MPE. It enables immediate intrapulmonary thrombolysis, which seems to be an effective therapeutic alternative in our group of patients with obstructive shock.
Aged↗
Adverse effects of interrupting precordial compression during cardiopulmonary resuscitation.
OBJECTIVES: In the current operation of automated external defibrillators, substantial time may be consumed for a "hands off" interval during which precordial compression is discontinued to allow for automated rhythm analyses before delivery of the electric countershock. The effects of such a pause on the outcomes of cardiopulmonary resuscitation were investigated. DESIGN: Prospective, randomized, controlled animal study. SETTING: Research laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Ventricular fibrillation was electrically induced in 25 Sprague-Dawley rats. After 4 mins of untreated ventricular fibrillation, precordial compression was begun and continued for 6 mins. Animals were then randomized to receive an immediate defibrillation shock or the defibrillation attempt was delayed for intervals of 10, 20, 30, or 40 secs. MEASUREMENTS AND MAIN RESULTS: Immediate defibrillation restored spontaneous circulation in each instance. When defibrillation was delayed for 10 or 20 secs, spontaneous circulation was restored in three of five animals in each group. After a 30-sec delay, spontaneous circulation was restored in only one of five animals (p < .05). No animal was successfully resuscitated after a 40-sec delay (p < .01). With increasing delays, 24- and 48-hr survival rates were correspondingly reduced. CONCLUSIONS: During resuscitation from ventricular fibrillation, prolongation of the interval between discontinuation of precordial compression and delivery of the first electric countershock substantially compromises the success of cardiac resuscitation. Accordingly, automated defibrillators are likely to be maximally effective if they are programmed to secure minimal "hands off" delay before delivery of the electric countershock.
Animals↗
Effectiveness of bystander CPR.
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Cardiopulmonary Resuscitation↗
Adrenergic vasopressor agents and mechanical ventilation for the treatment of experimental septic shock.
OBJECTIVE: Vasopressor agents and mechanical ventilation are routine interventions for the treatment of sepsis complicated by hypotension. It was our hypothesis that such treatment singly or in combination increases the duration of survival. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Thirty male Sprague-Dawley rats anesthetized with intraperitoneal injection of pentobarbital. INTERVENTIONS: Peritonitis was induced by cecal ligation and spillage of cecal contents into the abdominal cavity. The first phase of this study was performed on 15 spontaneously breathing Sprague-Dawley rats that were randomized to three groups of five animals each. One group received treatment with dopamine. The second group received norepinephrine. The third group received only the diluent as a placebo. Concentrations of the vasopressor agents were increased such that mean arterial pressure was maintained at approximately 80% of baseline values; the volumes infused were kept constant. For the second phase of this study, the grouping of animals and the techniques of study were identical, except that rats were mechanically ventilated. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure was best maintained with norepinephrine. However, no statistically significant differences in duration of survival, cardiac index, arterial blood lactate concentration, or arterial and venous PCO2 and PO2 values were identified between groups. With mechanical ventilation, survival was prolonged (p < .01). Survival was increased from an average of 291 mins to 342 mins with dopamine, from 257 mins to 352 mins in placebo controls, and from 280 mins to 329 mins with norepinephrine. Again, no significant differences in hemodynamic and blood gas measurements, or in the duration of survival between vasopressor-treated and control animals were documented. CONCLUSIONS: No benefit or detriment was demonstrated when vasopressor agents were administered to sustain arterial pressure in the course of experimental peritonitis in this murine model of septic shock. This finding contrasted with highly significant prolongation of survival when animals were mechanically ventilated. There was no evidence that routine vasopressor therapy, under these controlled experimental conditions in rats, improved duration of survival.
Adrenergic alpha-Agonists↗
Subacute rupture of the left ventricular free wall after acute myocardial infarction. Three cases of long-term survival without emergency surgical repair.
Rupture of the left ventricular free wall after acute myocardial infarction (AMI) has been regarded as uniformly fatal unless emergency surgical repair is performed. Among 2,862 patients admitted with AMI to our ICU during the last 8 years, 107 patients developed rupture of the left ventricular free wall. Twenty-nine patients had a subacute course and three of them survived for prolonged periods without having to have emergency surgical repair. At the onset of rupture on day 1 through 7 after AMI, the three survivors developed sudden hypotension accompanied by a new pericardial effusion. They were initially managed with hemodynamic support. Two patients had elective open-heart surgery 2 to 3 months after AMI, whereas one patient did nt require surgery. All three survived 1 1/2 to 8 1/2 years after AMI. This report indicates that a small subset of patients with subacute ventricular free wall rupture has a benign course that may allow for prolonged survival without having to have emergency surgical repair.
Aged↗
Epinephrine increases the severity of postresuscitation myocardial dysfunction.
BACKGROUND: Epinephrine has been the mainstay for cardiac resuscitation for more than 30 years. Its vasopressor effect by which it increases coronary perfusion pressure is likely to favor initial resuscitation. Its beta-adrenergic action, however, may have detrimental effects on postresuscitation myocardial function when administered before resuscitation because it increases myocardial oxygen consumption. In the present study, our focus was on postresuscitation effects of epinephrine when this adrenergic agent was administered during cardiopulmonary resuscitation. Postresuscitation myocardial functions were compared with those of a selective alpha-adrenergic agent, phenylephrine, when epinephrine was combined with a beta 1-adrenergic blocking agent, esmolol, and saline placebo. METHODS AND RESULTS: Ventricular fibrillation was induced in 40 Sprague-Dawley rats. Mechanical ventilation and precordial compression was initiated either 4 or 8 minutes after the start of ventricular fibrillation. The adrenergic drug or saline placebo was administered as a bolus after 4 minutes of precordial compression. Defibrillation was attempted 4 minutes later. Left ventricular pressure, dP/dt40, and negative dP/dt were continuously measured for an interval of 240 minutes after successful cardiac resuscitation. Except for saline placebo, comparable increases in coronary perfusion pressure were observed after each drug intervention. The number of countershocks required for restoration of spontaneous circulation was significantly greater for epinephrine-treated animals (10 +/- 8) when compared with phenylephrine-treated animals (1.8 +/- 0.4, P < .01) and with animals treated with epinephrine combined with esmolol (1.6 +/- 0.9, P < .01). After resuscitation, dP/dt40 and negative dP/dt were significantly decreased and left ventricular end-diastolic pressure was significantly increased in each animal when compared with prearrest levels. However, the greatest impairment followed epinephrine, and this was associated with significantly greater heart rate and the shortest interval of postresuscitation survival of 8 +/- 4 hours, whereas placebo controls survived for 12 +/- 11 hours. Phenylephrine-treated animals survived for 41 +/- 10 hours (P < .01 versus epinephrine), and animals that received a combination of epinephrine and esmolol survived for 35 +/- 11 hours (P < .01 versus epinephrine). When the duration of untreated cardiac arrest was increased from 4 to 8 minutes, the severity of postresuscitation left ventricular dysfunction was magnified, but disproportionate decreases in postresuscitation survival were again observed with placebo and epinephrine when compared with alpha-adrenergic agonists. CONCLUSIONS: In an established rodent model after resuscitation following cardiac arrest, epinephrine significantly increased the severity of postresuscitation myocardial dysfunction and decreased duration of survival. More selective alpha-adrenergic agonist or blockade of beta 1-adrenergic actions of epinephrine reduced postresuscitation myocardial impairment and prolonged survival.
Adrenergic Agonists↗
Mechanisms of myocardial hypercarbic acidosis during cardiac arrest.
During the global myocardial ischemia of cardiac arrest and during regional myocardial ischemia due to local impairment of coronary blood flow, intramyocardial carbon dioxide tensions (Pmco2) of ischemic myocardium increase to levels exceeding 400 Torr. The mechanism of such myocardial hypercarbic acidosis is as yet incompletely understood, specifically whether these increases in Pmco2 are due to increased oxidative metabolism, decreased CO2 removal, or buffering of metabolic acids. We therefore measured Pmco2 and the total CO2 content of rat hearts harvested before, during, and after resuscitation from cardiac arrest. Pmco2 significantly increased from an average of 63 to 209 Torr during a 4-min interval of untreated ventricular fibrillation. This was associated with concurrent decreases in intracellular pH from an average of 7.03 to 6.02 units. The total CO2 content of the myocardium simultaneously decreased from 17.0 to 16.5 mmol/kg. Accordingly, increases in Pmco2 and [H+] were observed in the absence of increases in the total CO2 content and therefore the calculated myocardial bicarbonate. These observations in the rat model implicate buffering of metabolic acids by bicarbonate rather than increases in CO2 production or decreases in CO2 removal as the predominant mechanism accounting for myocardial hypercarbia.
Acidosis↗
Mechanical ventilation may not be essential for initial cardiopulmonary resuscitation.
BACKGROUND: In a rodent model of cardiac arrest and resuscitation in which the inspired gas mixture was enriched with oxygen, resuscitability and survival were unaffected by positive pressure ventilation. In the present study, in a larger animal model, tidal volumes generated during precordial compression and with spontaneous gasping were quantitated. METHODS: Domestic pigs with an average weight of 34 kg were anesthetized with pentobarbital. Ventricular fibrillation (VF) was induced electrically. Precordial compression was begun after 4 min of untreated VF. Each of 22 animals received one of two interventions in conjunction with precordial compression: positive pressure ventilation with oxygen or oxygen supplied at the port of a tracheal tube at ambient pressure. After 8 min of precordial compression, defibrillation was attempted. RESULTS: Only very moderate increases in arterial PCO2 were documented during cardiopulmonary resuscitation in the absence of mechanical ventilation but arterial oxygen tension was consistently in excess of 100 mm Hg. Cardiac resuscitability and 48-h survival were approximately the same in animals maintained on inspired oxygen whether or not they were mechanically ventilated (7/11 or 8/11). In the absence of mechanical ventilation, precordial compression and spontaneous gasping yielded minute volumes that exceeded 5 L. CONCLUSION: Positive pressure mechanical ventilation did not improve resuscitability or postresuscitation outcome in this porcine model of cardiac arrest.
Animals↗
Spontaneous gasping increases the ability to resuscitate during experimental cardiopulmonary resuscitation.
OBJECTIVE: To evaluate the effect of spontaneous gasping on cardiorespiratory functions and the ability to resuscitate during experimental cardiac arrest. DATA SOURCES: Studies in rat and pig models during cardiac arrest and cardiopulmonary resuscitation (CPR). STUDY SELECTION: We retrospectively examined the role of spontaneous gasping during the course of experimental studies on cardiopulmonary resuscitation. DATA EXTRACTION: The data were extracted to illustrate the mechanisms of spontaneous gasping and its effects on pulmonary gas exchange and blood circulation during CPR. DATA SYNTHESIS: Spontaneous gasping increased PaO2 and decreased PaCO2 values during precordial compression in the absence of mechanical ventilation. The frequency of gasping during precordial compression was greater in successfully resuscitated animals. A significant linear correlation was established between coronary artery perfusion pressure and both the frequency (r2 = .90, p < .01) and the duration (r2 = 0.69, p < .01) of gasping during untreated ventricular fibrillation and before resuscitation was attempted. Like coronary perfusion pressure, the frequency and duration of gasping predicted the success of cardiac resuscitation attempts. CONCLUSIONS: Spontaneous gasping is associated with both pulmonary and hemodynamic effects during cardiac arrest in experimental animals. Spontaneous gasping is biologically useful and is predictive of a more favorable outcome of resuscitative efforts.
Animals↗
Gastric intramural PCO2 as monitor of perfusion failure during hemorrhagic and anaphylactic shock.
Indirect measurement of gastric intramural pH (pHG) utilizing a luminal tonometer in the stomach has been proposed for monitoring the severity and progression of perfusion failure. In the present study, we investigated gastric PCO2 and pHG as indicators and quantitators of the severity of perfusion failure in the experimental rodent model of both hemorrhagic and anaphylactic shock. Gastric intramural PCO2 (PGCO2) and pHG were directly measured with miniaturized sensors inserted into the anterior wall of the stomach. In hemorrhagic shock, animals were bled into a reservoir maintained at a pressure of 35 mmHg. pHG decreased from 7.39 +/- 0.08 to 6.67 +/- 0.11 (P < 0.01), and PGCO2 increased from 53 +/- 4 to 136 +/- 3 Torr (P < 0.01). Anaphylactic shock was induced in animals that had been sensitized 21 days before with crystallized ovalbumin. Antigen challenge produced an immediate reduction in mean aortic pressure from 144 to 60 mmHg. pHG decreased from 7.40 +/- 0.05 to 6.99 +/- 0.07 (P < 0.01), and PGCO2 increased from 48 +/- 5 to 133 +/- 9 Torr (P < 0.01). The increases in PGCO2 were highly correlated with decreases in gastric blood flow in both hemorrhagic (r = 0.96) and anaphylactic shock (r = 0.92). The correlations with pHG were more moderate. These experiments demonstrated prominent increases in PGCO2 and H+ during both hemorrhagic and anaphylactic shock. We further noted that the estimation of pHG based on the assumption that HCO3-concentrations of the stomach wall and arterial blood are the same was not fully sustained.
Anaphylaxis↗