Left ventricular performance after acute myocardial infarction

Karliner, Joel S.; Ross, John

doi:10.1016/s0033-0620(71)80013-0

Cited by 44 publications

(7 citation statements)

References 101 publications

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“…Although patients with cardiogenic shock frequently demonstrate several small foci of necrotic myocardial cells throughout the left ventricle (Page el Alonso et al, 1973) they usually have one major infarcted area. Nevertheless, the haemodynamic characteristics of the model presented are in most ways similar to the haemodynamic features of patients with acute left ventricular failure due to myocardial infarction (Hamosh & Cohn, 1971 ;Karliner & Ross, 1971). This model however, may not be valid for myocardial insufficiency of non-ischaemic etiology.…”

Section: Discussionmentioning

confidence: 85%

“…The main cause of death in patients hospitalized for acute myocardial infarction is progressive cardiac decompensation or cardiogenic shock (Swan et al, 1970). In pump failure preceding shock, left ventricular performance is markedly depressed as evidenced by elevated left ventricular end-diastolic pressure and reduced cardiac output, while blood pressure often is maintained due to increased total peripheral resistance (Hamosh & Cohn, 1971 ;Karliner & Ross, 1971). The aim of the present investigation was to develop an animal model showing the haemodynamic and metabolic signs of acute left ventricular pump failure, the stage before cardiogenic shock.…”

Section: Introductionmentioning

confidence: 99%

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A reproducible and stable model of acute ischaemic left ventricular failure in dogs

Smiseth

Mjøs

1982

Clinical Physiology

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A model of acute ischaemic left ventricular (LV) failure is presented. In closed-chest anaesthetized dogs 50 micrometer plastic microspheres were injected repeatedly into the left main coronary artery over a period of about 40 min. The injections effected stepwise elevations of LV end-diastolic pressure (LVEDP). Thus, LVEDP could be increased to a desired level, about 20 mmHg, in a very controlled manner. All dogs developed signs of markedly depressed LV performance. Haemodynamic conditions stabilized about 60 min after embolization. The maximum LVDP/dt decreased from 2696 +/- 169 to 1823 +/- 98 mmHg . x-1, cardiac output decreased from 2.81 +/- 0.20 to 1.98 +/- 0.14 l . min-1 and mean aortic blood pressure decreased from 144 +/- 4 to 127 +/- 3 mmHg, while total peripheral resistance increased from 56 +/- 3 to 69 +/- 3 mmHg . l-1 . min. Myocardial blood flow decreased from 103 +/- 7 to 79 +/- 6 ml . min-1 . 100 g-1 and myocardial oxygen consumption decreased from 12.5 +/- 0.9 to 8.3 +/- 0.8 ml . min-1. 100 g-5. Myocardial uptake of lactate and free fatty acids decreased markedly. Electrocardiography showed signs of acute ischaemia. There were no deaths due to ventricular fibrillation. Morphological studies showed multiple small infarcts throughout the entire LV. In conclusion, repeated coronary embolization with 50 micrometers plastic microspheres, guided by the rise of LVEDP represents a simple and reproducible method for induction of uniform and stable acute LV failure.

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Section: Discussionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

A reproducible and stable model of acute ischaemic left ventricular failure in dogs

Smiseth

Mjøs

1982

Clinical Physiology

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“…In addition to the fact that good chest films are logistic-ally difficult to obtain, determination of P terminal force has the advantage of being a sensitive monitor of the adequacy of fluid therapy in terms of an optimal filling pressure of the left side of the heart. Clinical and haemodynamic correlations A rise in the LV end-diastolic pressure has been reported to occur in the majority of patients with acute myocardial infarction even when uncomplicated (Hunt et al, 1970;Hamosh and Cohn, I97I;Karliner and Ross, 197I;Rahimtoola et al, I97I). However, the mean ('pre-a') LV filling pressure and the mean left atrial pressure has a closer association with the development of pulmonary venous hypertension than the higher but instantaneous LV end-diastolic pressure which is greatly influenced by alteration of myocardial compliance.…”

Section: Discussionmentioning

confidence: 99%

Prediction of left heart filling pressure and its sequential change in acute myocardial infarction from the terminal force of the P wave.

Heikkilä¹,

Hugenholtz²,

Tabakin³

1973

Heart

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Left ventricular filling pressure serves as a most useful haemodynamic index of cardiac dysfunction in acute myocardial infarction. In order to predict the filling pressure from the P wave of the electrocardiogram,flowdirected Swan-Ganz catheters were inserted in 40 acutely ill patients (36 with acute myocardial infarction or serious angina). An elementary electrocardiographic measurement, the P terminal force in lead Vi was found to be well and inversely correlated to the level of mean left ventricular filling pressure, particularly in patients with acute left heart failure (P< o ooI, r= -o82). Significant correlation (P< o ooI) was further noted between left ventricular filling pressure and clinical severity of acute myocardial infarction, mixed venous oxygen saturation, pulmonary radles, and radiological pulmonary vascular congestion. Absence of third andfourth heart sounds indicated normal left ventricularfilling pressure in acute myocardial infarction but the reverse was not found to be true. Acute sequential variations in left ventricular filling pressure were paralleled by the P terminal force more closely than any other recorded variable.It is concluded that P wave alterations provide a useful, simple, and noninvasive toolfor quantitative assessment of acute changes in LV preload in seriously ill patients.

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“…These data under score the fact that subsequent left ventricular dysfunction in individual patients cannot always be predicted by the site or type of myocardial infarc tion. Rather, total infarct size is most likely the best predictor of subsequent left ventricular performance and an important indicator of overall prognosis [81-Several investigators [11][12][13][14][15] have studied left ventricular function fol lowing acute myocardial infarction in man, but there have been few studies documenting actual changes in left ventricular performance prior to and following infarction. Stewart et al…”

Section: Discussionmentioning

confidence: 99%

Serial Angiographic Studies before and after Acute Myocardial Infarction in Man

Buda¹,

Macdonald²

1981

Cardiology

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In this study, 6 patients underwent angiographic assessment prior to and subsequent to acute myocardial infarction. The mean inter-angiographic interval was 36 months and the mean infarct to angiography interval was 8 months. Left ventricular ejection fraction decreased from 0.69 to 0.45 after infarction. The degree of left ventricular dysfunction after infarction did not necessarily relate to the site or type of infarction. All patients had significant progression of their coronary lesions with occlusion of a major coronary vessel in the interval. Coronary artery occlusion with infarction produces a variable degree of damage and subsequent left ventricular dysfunction.

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Left ventricular performance after acute myocardial infarction

Cited by 44 publications

References 101 publications

A reproducible and stable model of acute ischaemic left ventricular failure in dogs

A reproducible and stable model of acute ischaemic left ventricular failure in dogs

Prediction of left heart filling pressure and its sequential change in acute myocardial infarction from the terminal force of the P wave.

Serial Angiographic Studies before and after Acute Myocardial Infarction in Man

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