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Rupture of the left ventricular myocardium during the course of an acute myocardial infarction may affect the free wall, the interventricular septum, or the papillary muscles. When a rupture occurs, it is referred to as a mechanical complication of acute myocardial infarction. All mechanical complications may lead to cardiogenic shock. However, the location of the rupture can often be suspected clinically. To confirm the diagnosis, echocardiography must be performed. Since the advent of thrombolytic therapy and percutaneous coronary intervention, the incidence of mechanical complications has declined. Even though mortality remains high, their recognition is important since survivors may have an excellent long-term prognosis. The cases convey two main messages: 1) Mechanical complications must be carefully searched for in any patient with an acute coronary syndrome and signs of cardiogenic shock and/or a systolic murmur. 2) Aggressive and timely medical and surgical treatment should be provided even though in a substantial proportion of these patients prognosis may be dismal.

Despite new insights into mechanisms contributing to ischemia-reperfusion injury, new therapeutic interventions to reduce ischemia-reperfusion injury have thus far not been available for routine clinical use. In order to restore sufficient postischemic contractile function, such a therapy would be of great value in conjunction with reperfusion therapy for acute myocardial infarction and after cardiac surgery. This paper examines whether metabolic disturbances and energy depletion contribute to ischemia-reperfusion injury and whether metabolic interventions could alleviate ischemia-reperfusion injury. Experimental and clinical studies are reviewed for evidence of a beneficial effect of metabolic interventions, in particular of increased glycolytic substrate, on ischemia-reperfusion injury. During ischemia, metabolism of the myocardium shifts to a preferential use of carbohydrates. Increased glycolytic substrate i.e. glucose-insulin-potassium infusion as metabolic support for ischemic myocardium is beneficial in reducing ischemia-reperfusion injury by increasing energy production via anaerobic glycolysis, decreasing circulating free fatty acids and intracellular free fatty acid accumulation, maintaining ion homeostasis, reducing cellular edema, and scavenging free radicals. During reperfusion, glucose-insulin-potassium, apart from increasing glycolysis and decreasing free fatty acid metabolism, provides substrate for replenishment of the citric acid cycle, which is important for optimal energy transfer. During ischemia, glucose-insulin-potassium preserves energy reserves and maintains cell viability. During reperfusion, glucose-insulin-potassium improves energy transfer and increases contractile function. Experimental and clinical studies have proven glucose-insulin-potassium to be a safe and effective intervention to reduce ischemia-reperfusion injury.

The recovery of systolic and diastolic function during unstable angina may be modified by the repetition of brief episodes of ischemia and by the presence of left ventricular hypertrophy (LVH). We studied the effects of six consecutive 5-minute cycles of no-flow ischemia and reperfusion followed by 25 minutes of recovery in isovolumic red blood cell-perfused hearts from aortic-banded rats with chronic LVH (n = 8) and sham-operated control rats (n = 8). At baseline (left ventricular end-diastolic pressure [LVEDP], 10 mm Hg), left ventricular developed pressure (123 +/- 5 versus 114 +/- 5 mm Hg/g) and coronary flow [2.5 +/- 0.3 versus 2.2 +/- 0.2 (mL/min)/g] were similar in LVH versus control rats. Repetitive ischemia was associated with progressive depression of postischemic recovery of left ventricular systolic function, and the recovery of left ventricular developed pressure after the final 25-minute reperfusion period was similar in LVH versus control rats (61 +/- 6% versus 72 +/- 4% of baseline, P = NS). Although there was no increase in isovolumic LVEDP during the initial cycle of transient ischemia, both groups showed a rapid and similar rise in LVEDP during subsequent ischemic cycles (delta 82 +/- 8 versus delta 89 +/- 7 mm Hg/g in response to the final ischemia cycle for LVH versus control rats, respectively; P = NS). The control hearts showed complete restoration of LVEDP to baseline during final reperfusion, whereas the LVH hearts showed prolonged and severe postischemic diastolic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

We studied the effects of angiotensin II during low-flow ischemia and reperfusion using red cell-perfused isovolumic rabbit hearts. Under baseline conditions where coronary perfusion pressure (CPP) was 100 mm Hg and left ventricular end-diastolic pressure (LVEDP) was set at 10 mm Hg, 10(-8) M angiotensin II caused a mild increase in LV developed pressure (+12%) and decrease in coronary flow (-8%). Low-flow ischemia was imposed by reducing CPP to 15 mm Hg for 30 min followed by 30 min of reperfusion. During ischemia, the angiotensin II group showed a gradual further reduction in coronary flow in association with a greater depression of LV developed pressure and increase in LVEDP relative to the no-drug group. To separate the effect of angiotensin II on coronary flow from a direct myocardial effect, the angiotensin II group was compared with an additional no-drug group with a matched progressive reduction in coronary flow during ischemia. In these groups, the ischemic depression of LV developed pressure, myocardial ATP levels, and lactate production were similar. However, the ischemic rise in LVEDP was greater (42.0 +/- 5.4 vs. 19.9 +/- 1.3 mm Hg, P less than 0.01) and recovery was incomplete in the angiotensin II group. These observations suggest that angiotensin II exerts a direct adverse effect on LV diastolic relaxation during low-flow ischemia and recovery.

Patients with mitral or aortic valve disease constitute an important part of patients in cardiology practice. General practitioners and internists have an important role in the long-term care of these patients. We review current knowledge and recommendations for follow-up, medical therapy and indications for surgery in patients with aortic and mitral valve disease. Asymptomatic patients with valve disease need a clinical and echocardiographic follow-up at specific time intervals. Most patients with mild or moderate valve disease do not need medical or surgical therapy. However, once a patient becomes symptomatic, he needs a non-invasive and likely an invasive evaluation for surgical valve repair or replacement. In case the valve disease progresses without the development of clinical symptoms, the indication for surgery must be derived from hemodynamic parameters, the onset of arrhythmias (atrial fibrillation), and pulmonary hypertension. In symptomatic and asymptomatic severe valve disease specific medical therapy can be very beneficial. However, improvement under medical therapy should not delay a prognostically necessary surgical valve repair or replacement.

Rupture of the left ventricular myocardium during the course of an acute myocardial infarction may affect the free wall, the interventricular septum, or the papillary muscles. When a rupture occurs, it is referred to as a mechanical complication of acute myocardial infarction. All mechanical complications may lead to cardiogenic shock. However, the location of the rupture can often be suspected clinically. To confirm the diagnosis, echocardiography must be performed. Since the advent of thrombolytic therapy and percutaneous coronary intervention, the incidence of mechanical complications has declined. Even though mortality remains high, their recognition is important since survivors may have an excellent long-term prognosis. The cases convey two main messages: 1) Mechanical complications must be carefully searched for in any patient with an acute coronary syndrome and signs of cardiogenic shock and/or a systolic murmur. 2) Aggressive and timely medical and surgical treatment should be provided even though in a substantial proportion of these patients prognosis may be dismal.

Vasovagal episodes occur frequently in young healthy patients undergoing venous cannulation and loco-regional anaesthesia. We report two cases of severe coronary vasospasm and non-Q-wave infarction in healthy young women after administration of ephedrine for vasovagal symptoms at the onset of spinal anaesthesia. In the light of unopposed vagal predominance pre-disposing patients to coronary vasospasm, even in young healthy patients, atrophine and not ephedrine should be the first line treatment for bradycardia with or without hypotension under spinal anaesthesia.

Vasovagal episodes occur frequently in young healthy patients undergoing venous cannulation and loco-regional anaesthesia. We report two cases of severe coronary vasospasm and non-Q-wave infarction in healthy young women after administration of ephedrine for vasovagal symptoms at the onset of spinal anaesthesia. In the light of unopposed vagal predominance pre-disposing patients to coronary vasospasm, even in young healthy patients, atrophine and not ephedrine should be the first line treatment for bradycardia with or without hypotension under spinal anaesthesia.

We sought to determine the pathogenetic predictors of collateral channels in a large cohort of patients with coronary artery disease (CAD).The frequency distribution of collateral flow in patients with CAD is unknown. Only small qualitative studies have investigated which factors influence the development of collateral channels.In 450 patients with one- to three-vessel CAD undergoing percutaneous transluminal coronary angioplasty (PTCA), collateral flow was measured. A collateral flow index (CFI; no unit) expressing collateral flow relative to normal anterograde flow was determined using coronary wedge pressure or Doppler measurements through sensor-tipped PTCA guide wires. Frequency distribution analysis of CFI and univariate and multivariate analyses of 32 factors, including gender, age, patient history, cardiovascular risk factors, medication and coronary angiographic data, were performed.Two-thirds of the patients had a CFI0.25 and approximately 40% of patients had a CFI0.15, but only approximately 10% of the patients had a recruitable CFIor =0.4. By univariate analysis, the following were predictors of CFIor =0.25: high levels of high-density lipoprotein cholesterol, the absence of previous non-Q-wave myocardial infarction, angina pectoris during an exercise test, angiographic indicators of severe CAD and the left circumflex or right coronary artery as the collateral-receiving vessel. Percent diameter stenosis of the lesion undergoing PTCA was the only independent predictor of a high CFI.This large clinical study of patients with CAD in whom collateral flow was quantitatively assessed reveals that two-thirds of the patients do not have enough collateral flow to prevent myocardial ischemia during coronary occlusion, and that coronary lesion severity is the only independent pathogenetic variable related to collateral flow.

Anomalous origin of the coronary arteries is infrequent and a single coronary artery is seen even less frequently. Accordingly, few reports have described percutaneous coronary interventions in this anomaly. We report successful balloon angioplasty and stenting of a left main trunk originating from the right coronary artery.

Mechanical compression of coronary artery stents may be associated with a fatal outcome as the result of refractory myocardial ischemia. We present the history of an 83-yr-old patient, who died owing to hemorrhagic shock 3 days after stent implantation, despite immediate cardiopulmonary resuscitation (CPR). Postmortem examination showed stent compression, probably due to mechanical deformation during CPR. This complication has been reported in two other cases in the literature, suggesting that CPR may be hazardous to patients with coronary artery stents.

The coronary collateral circulation is an alternative source of blood supply to a myocardial area jeopardized by the failure of the stenotic or occluded vessel to provide enough blood flow to this region. Until recently, only qualitative or semiqualitative methods have been available for the assessment of the coronary collateral circulation in humans, such as the patient's history of walk-through angina pectoris, the registration of intracoronary ECG signs for myocardial ischaemia or angina pectoris during coronary occlusion, or coronary angiographic classification (score 0-3) of collaterals. Studies of coronary wedge pressure measurements distal of a balloon-occluded coronary artery and the recent advent of ultrathin pressure and Doppler angioplasty guidewires have made it possible to obtain pressure or flow velocity data in remote vascular areas and, thus, to calculate functional variables for coronary collateral flow. Those coronary occlusive pressure- and flow velocity-derived parameters express collateral flow as a fraction of antegrade coronary flow during vessel patency of the collateral-receiving vessel. They are both interchangeable, and they have been validated in comparison to 'traditional' methods and against each other. The possibility of accurately measuring coronary collateral flow indices in humans undergoing coronary balloon angioplasty opens areas of investigation of the pathogenesis, pathophysiology and therapeutic promotion of the collateral circulation previously reserved for exclusively experimental studies. The purpose of this article is to review several clinically available methods for the functional characterization of the coronary collateral circulation.

The terms “acute hibernation” and “short-term hibernation” may seem oxymoronic since “hibernation” implies a prolonged period of dormancy and subsequent reawakening. Nonetheless, the concept of acute hibernation has provided a useful framework for research studies involving relatively brief periods of low flow or moderate ischemia which depress myocardial function but do not cause homogeneous irreversible injury; therefore significant recovery or “reawakening” of the ischemically depressed myocardium can occur with reperfusion. The sequence of relatively brief ischemia followed by reperfusion has obvious relevance to clinical scenarios of unstable angina, acute coronary thrombosis and impending myocardial infarction which is treated with thrombolytic therapy, and the ischemia-reperfusion sequence which accompanies cardiac surgery. The mechanisms regulating acute hibernation during low-flow ischemia and recovery during reperfusion merit serious investigation because of their clinical relevance and potential for beneficial therapeutic manipulation.

Percutaneous transvenous mitral valvuloplasty using the double-balloon technique has been attempted in 25 patients (mean age 39 +/- 10 years; 17 women, 8 men) with severe, non-calcified (20 patients) or only slightly calcified (5 patients) mitral stenosis. Valvuloplasty was successful in 22 of the 25 patients. The procedure resulted in a marked increase in mitral valve area from 1.0 +/- 0.2 to 1.9 +/- 0.5 cm2 (p0.001) whereas the diastolic transmitral gradient decreased from 11 +/- 4 to 4 +/- 2 mm Hg (p0.001). Functional classification according to the New York Heart Association improved from 2.4 +/- 0.6 to 1.7 +/- 0.5 (p0.001) and physical working capacity increased from 64 +/- 20 to 76 +/- 17% (p0.01). In 3 patients the procedure was not successful: cardiac tamponade and ventricular perforation occurred in 1 patient each and in the third valvuloplasty had to be ended because of lack of cooperation. Follow-up examination was performed 24 +/- 17 months after successful valvuloplasty. In all patients an electrocardiogram, an exercise test and an echocardiogram were obtained after 3, 12, 26 and 40 months. Sinus rhythm was found in 13 and atrial fibrillation in 9 patients before valvuloplasty. After the procedure 3 additional patients could be converted into sinus rhythm. Physical exercise capacity did not change during the follow-up. Mitral valve area determined by Doppler-echocardiography increased from 1.0 +/- 0.1 to 1.7 +/- 0.3 cm2 (p0.001) after valvuloplasty and decreased slightly to 1.5 +/- 0.2 cm2 (NS) during the follow-up. Left atrial chamber diameter did not change significantly after the procedure (5.2 vs. 5.0 cm). It is concluded that percutaneous mitral valvuloplasty is successful in 88% of all patients with severe, non calcified mitral stenosis. The clinical result seems to be beneficial and almost all patients had a stable follow-up for two years. Several complications during the procedure occurred in two patients (8%).

To assess the value of late potential recordings in predicting complex ventricular arrhythmias in chronic coronary heart disease, signal-averaged ECG and 24-h Holter were performed in 101 consecutive patients following coronary arteriography. In 69 of 101 patients, non-sustained ventricular tachycardia (VT) (22 patients) or monotopic or polytopic ventricular premature beats (VPB) (47 patients) were detected. When the different patient groups (VT, VPB, no arrhythmias) were compared, the parameters defining the late potentials demonstrated broad variability. Patients with non-sustained ventricular tachycardia showed a tendency to increased late potentials, though this tendency was not significant. In patients with pathologic late potentials the predictability of non-sustained ventricular tachycardia was only 38%. - It is therefore concluded that late potentials in patients with chronic coronary heart disease are not directly linked to the extent and severity of arrhythmias recorded in the ambulatory 24-h Holter.

ACCF : American College of Cardiology Foundation ACS : acute coronary syndrome AHA : American Heart Association CAD : coronary artery disease CABG : coronary artery bypass grafting CKMB : creatine kinase MB isoform cTn : cardiac troponin CT : computed tomography CV : coefficient of variation ECG : electrocardiogram ESC : European Society of Cardiology FDG : fluorodeoxyglucose h : hour(s) HF : heart failure LBBB : left bundle branch block LV : left ventricle LVH : left ventricular hypertrophy MI : myocardial infarction mIBG : meta-iodo-benzylguanidine min : minute(s) MONICA : Multinational MONItoring of trends and determinants in CArdiovascular disease) MPS : myocardial perfusion scintigraphy MRI : magnetic resonance imaging mV : millivolt(s) ng/L : nanogram(s) per litre Non-Q MI : non-Q wave myocardial infarction NSTEMI : non-ST-elevation myocardial infarction PCI : percutaneous coronary intervention PET : positron emission tomography pg/mL : pictogram(s) per millilitre Q wave MI : Q wave myocardial infarction RBBB : right bundle branch block sec : second(s) SPECT : single photon emission computed tomography STEMI : ST elevation myocardial infarction ST–T : ST-segment –T wave URL : upper reference limit WHF : World Heart Federation WHO : World Health Organization Myocardial infarction (MI) can be recognised by clinical features, including electrocardiographic (ECG) findings, elevated values of biochemical markers (biomarkers) of myocardial necrosis, and by imaging, or may be defined by pathology. It is a major cause of death and disability worldwide. MI may be the first manifestation of coronary artery disease (CAD) or it may occur, repeatedly, in patients with established disease. Information on MI rates can provide useful information regarding the burden of CAD within and across populations, especially if standardized data are collected in a manner that …