Holter electrocardiographic recording: Part 2, Current indications and applications.
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Biomedical subjects
Publications and source records attributed to D R Taylor.
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It has been shown previously that 30-minute infusions of intravenous nitroglycerin in patients with acute myocardial infarction are able to lower left ventricular filling pressure and improve left ventricular function while lowering mean arterial pressure by only 7 mmHg (0.9 kPa). A decrease in sigmaST in praecordial ST segment mapping studies during nitroglycerin infusion in patients with anterior infarction suggested a decrease in the extent of myocardial ischaemia. In the present study, 30 patients with acute myocardial infarction received 1- to 3-hour infusions of intravenous nitroglycerin at infusion rates sufficient to lower mean arterial pressure by an average of 22 mmHg (2.9 kPa). An improvement in ventricular function was noted in that subgroup of patients with the msot severe left ventricular dysfunction. All patients with anterior myocardial infarction underwent serial ST segment mapping and, irrespective of the presence or absence of left ventricular failure, showed a decrease in sigmaST during nitroglycerin infusion (P less than 0.005). These findings suggest that infusion of nitroglycerin improves left ventricular function and/or alters left ventricular compliance in patients with left ventricular failure complicating myocardial infarction and furthermore decreases sigmaST in all patients, irrespective of the presence or absence of left ventricular failure, suggesting that the extent of myocardial ischaemia is decreased.
Fourteen patients with acute myocardial infarction were given 0.3 mg sublingual nitroglycerin within the first 12 hours of their acute myocardial infarction. Five minutes after sublingual nitroglycerin mean arterial pressure fell 9 mmHg (1.2 kPa) and remained significantly reduced for 30 minutes. Pulmonary capillary wedge pressure fell from a mean control value of 17 to 12 mmHg (2.3 to 1.6 kPa) and also remained reduced for 30 minutes. Heart rate was significantly raised and stroke work index reduced at five minutes. Patients with a stroke work index of greater than 55 g m per m-2 b.s.a. responed to nitroglycerin with a fall in both pulmonary capillary wedge pressue and strokework index while in those with a stroke work index of less than 55 g m per m-2 b.s.a. stroke work index did not fall concomitantly with the fall in pulmonary capillary wedge pressure. In one patient, nitroglycerin led to a precipitious fall in arterial pressure andrecurrence of chest pain.
Vasodilator therapy has been shown to improve ventricular function in patients with left ventricular failure complicating acute myocardial infarction. Sublingual nitroglycerin also improves ventricular function in these patients but its effects are transient and variable. Infusion of intravenous nitroglycerin in 12 patients with acute infarction resulted in a decrease in left ventricular filling pressure from a mean of 22 plus or minus 2 mm Hg to 12 plus or minus 1 mm Hg (P less than 0.001) associated with a 7 mm Hg decrease in mean arterial pressure (P less than 0.05). Since stroke work index did not change significantly, this represents and improvement in ventricular performance and/or an alteration in ventricular compliance. All six patients in whom serial precordial mapping studies were performed showed a decrease in sigma ST (P less than 0.001). These findings suggest that intravenous nitroglycerin improved left ventricular function and decreased the extent of myocardial ischemia. Longer infusion may act to preserve borderline ischemic myocardium and thus limit infarct size.
One hundred and eleven patients with transmural (TMI) and 49 with nontransmural myocardial infarction (NTMI) underwent hemodynamic investigation within 24 hours of onset of symptoms. Patients with NTMI were subdivided into those with ST-segment or T-wave changes alone with a normal QRS complex (NTMI-A) and a group with QRS abnormalities that did not satisfy the criteria for TMI (NTMI-B). Those with TMI had a significantly higher peak creatine phosphokinase (CPK) than those with NTMI: 840 plus or minus 99 and 336 plus or minus 69, respectively, P smaller than 0.05. There was not difference in peak CPK between those with NTMI-A and B. The incidence of arrhythmias and cardiac failure, and routine hemodynamic findings except for left ventricular filling pressure were similar in those with TMI and NTMI. There was not significant difference in in-hospital mortality between those with TMI (22%) and NTMI (33%). There was however a significant difference in in-hospital mortality between those with NTMI-A (0%) and NTMI-B (27%, P smaller than 0.05). The late mortality in those surviving their initial hospitalization was also not different between those with TMI (18%) and NTMI (19%) during a mean follow-up period of 20.2 months. In contrast to the in-hospital mortality those with NTMI-A had a late mortality similar to those with NTMI-B and those with TMI.
Twenty-seven patients with acute myocardial infarction not complicated by cardiogenic shock and ten normal volunteers were studied with gated cardiac blood pool scans. The ratio right vetricular area/left ventricular area (RVA/LVA) determined from the left anterior oblique end-diastolic scans was examined. The ratio was 1.11 +/- .06 in the normal volunteers. In patients with anterior infarction the ratio fell to 0.75 +/- .12 (P less than .05) due to left ventricular enlargement. In those with inferior infarction the ratio was 1.12 +/- .23 which was greater than in those with anterior infarction (P less than .05) due to enlargement of both the left and right ventricles. Six patients with cardiogenic shock, three with inferior and three with anterior infarction were studied. The three with anterior infarction had left ventricular enlargement and a decrease in the ratio of RVA/LVA to 0.62 while the three with inferior infarction had an increase in the ratio to 2.05 suggesting right ventricular dilatation and dysfunction. These studies suggest a high incidence of right ventricular dysfunction in patients with inferior myocardial infarction.
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