The nature of the pathologic lesion in sudden cardiac ischemic death is in dispute. Among 100 subjects who died of ischemic heart disease in less than six hours, coronary thrombi were found in 74. There was no difference in incidence between those who died in less than 15 minutes, those who died in 15 to 60 minutes, and those who died after one hour. Among 26 cases without an intraluminal thrombus, plaque fissuring was found in 21; thus, in only 5 cases was no acute arterial lesion demonstrated. No intraluminal thrombi were found in age-matched controls. Forty-eight of the 74 thrombi were found at sites of preexisting high-grade stenosis; 14 were found at points of previous stenosis of less than 50 per cent of the diameter of the lumen. Forty-seven per cent of the thrombi were found in the right coronary artery. Only 30 per cent were found in the left anterior descending coronary artery. The pathologic process in sudden ischemic death involves a rapidly evolving coronary-artery lesion in which plaque fissuring and resultant thrombus formation are present. These findings have implications for the prevention of sudden cardiac death by antithrombotic therapy.

Thrombosis and Acute Coronary-Artery Lesions in Sudden Cardiac Ischemic Death

Pathological and clinical studies have suggested that platelets have a role in the pathogenesis of unstable angina and myocardial infarction. However, the relation of platelet activation to episodic ischemia in patients with unstable angina is unknown. We assessed the biosynthesis of thromboxane and prostacyclin as indexes of platelet activation in patients with stable and unstable coronary disease by physicochemical analysis of metabolites in plasma and urine. Prostacyclin biosynthesis was markedly elevated in patients with acute myocardial infarction and correlated with plasma creatine kinase (r = 0.795; P less than 0.001). The largest rise in thromboxane synthesis was observed in patients with unstable angina, in whom 84 percent of the episodes of chest pain were associated with phasic increases in the excretion of thromboxane and prostacyclin metabolites. However, 50 percent of such increases were not associated with chest pain, possibly reflecting silent myocardial ischemia. These data indicate that platelet activation occurs during spontaneous ischemia in patients with unstable angina. The increment in prostacyclin biosynthesis during such episodes may be a compensatory response of vascular endothelium that limits the degree or effects of platelet activation. If so, biochemically selective inhibition of the synthesis or action of thromboxane A2 would be desirable in the treatment of unstable angina. In contrast, thromboxane inhibitors or antagonists would not be expected to be effective in patients with chronic stable angina, in whom there was no increase in the formation of thromboxane A2.

Platelet activation in unstable coronary disease.

Extensive microscopic examination of epicardial arteries and myocardium was performed in 25 cases of sudden death due to acute coronary thrombosis. Eighty-one percent of the thrombi had a layered structure with thrombus material of differing age, indicating that they were formed successively by repeated mural deposits that caused progressive luminal narrowing over an extended period of time. This episodic growth of the thrombus was accompanied by intermittent fragmentation of thrombus in 73% of the cases, with peripheral embolization causing microembolic occlusion of small intramyocardial arteries associated with microinfarcts. The period of unstable angina before the final heart attack was, in all but one of 15 patients, characterized by such an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation seemed to have alternated with intermittent thrombus fragmentation. The culmination of this "dynamic" thrombotic process in total vascular occlusion caused the final infarction and/or sudden death.

Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion.

To visualize intracoronary lesions in patients with different clinical expressions of coronary disease, we performed coronary angioscopy during coronary-artery bypass surgery in 10 patients with unstable angina and 10 patients with stable coronary disease. We examined a total of 32 vessels, using flexible fiberoptic angioscopes. Twenty-two vessels had no acute intimal lesion; three had complex plaques, six had thrombi, and one had both. Coronary angiography correctly identified the absence of complex plaque and thrombus in 22 vessels, but it detected only one of four complex plaques and one of seven thrombi. On angioscopy, none of the 17 arteries in the patients with stable coronary disease had either a complex plaque or thrombus. In the "offending" arteries of the patients with unstable angina, all three patients with accelerated angina had complex plaques and all seven with angina at rest had thrombi. We conclude that angioscopy frequently reveals complex plaques or thrombi not detected by coro...

Coronary Angioscopy in Patients with Unstable Angina Pectoris

Angiographie morphology and the pathogenesis of unstable angina pectoris

Although intracoronary thrombus formation plays a major role in acute transmural myocardial infarction (MI), its occurrence in unstable angina (UA) and nontransmural MI has not clearly been established. To determine whether intracoronary thrombus does occur in these syndromes, coronary arteriography was performed before, during, and after intracoronary nitroglycerin and streptokinase infusion in 17 patients. None of the 8 patients with nontransmural MI and 1 of the 9 patients with UA responded to intracoronary nitroglycerin. Seven of 8 patients with nontransmural MI and 4 of 9 patients with UA responded to streptokinase infusion with opening of an occluded vessel, an increase in stenotic diameter, dissolution of an intracoronary filling defect, or a combination of these. Serial opening and closing of ischemia-related vessels occurred spontaneously and in response to streptokinase in some patients in whom thrombolysis was demonstrated. Evidence of thrombolysis was not seen in any patient studied longer than 1 week from the onset of the rest pain syndrome. The finding of thrombolysis in several patients with nontransmural MI and UA suggests that intracoronary thrombus formation plays a pathogenetic role in some patients with these ischemic syndromes.

Intracoronary thrombus in nontransmural myocardial infarction and in unstable angina pectoris

Tachycardia upon swallowing. Evidence for a left atrial automatic focus.


 
 
 Type of funding sources: None.
 
 
 
 Despite the known benefits of physical activity, patients with cardiovascular disease do not practice enough nor maintain a regular physical activity for their health [1-4] . Walking is one of the easiest ways to stay physically active and can be implemented easily in everyday life [5]. Wearable physical activity monitoring devices have the potential to help increase physical activity through self-monitoring and feedback.
 
 
 
 To review randomized controlled trials using wearable physical activity monitoring device as an intervention to increase daily walking activity and improve physical capacities in cardiovascular diseases (CVD) patients.
 
 
 
 Design: Systematic review and meta-analysis of randomized controlled trials (RCTs).
 Data Sources: PubMed, Embase, Web of Science.
 Eligibility criteria: Randomized controlled studies including patients over 18 years of age with CVD comparing an intervention group using a wearable physical activity monitoring device with feedback to usual care or to a control group receiving no feedback on their physical activity and reporting a change in the daily number of steps and/or a change in the distance covered in the 6-minute walking test (6MWT) or a change in peak oxygen uptake (VO2 peak).
 Outcomes: Primary outcome was daily number of steps, secondary ouctomes were distance covered in the 6-minute walking test (6MWT) and/or peak oxygen uptake (VO2 peak).
 
 
 
 Sixteen RCTs were included. The intervention of wearing a physical activity monitoring device with feedback significantly improved daily number of steps compared with controls (standardized mean difference ((SMD) 0.85; 95% CI [0.42; 1.27], p < 0.01). The effect was greater when the duration of the intervention was less than 3 months (SMD 1.0; 95% CI [0.18; 1.82], p < 0.01) than when the duration of the intervention was 3 months or longer (SMD 0.71; 95% CI [0.27; 1.16], p < 0.01) but no significant interaction was found between subgroups (p = 0.55). Six MWT distance and VO2 peak showed only small effects (SMD 0.34 (95% CI [-0.11; 0.80], p = 0.02) and SMD 0.53 (95% CI [0.03; 1.03], p = 0.07), respectively).


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Impact of wearable devices with feedbacks for increasing daily walking activity and physical capacities in cardiovascular patients: a meta-analysis of randomized controlled trials

Steven M. Laporte

Papers

Intracoronary thrombus in nontransmural myocardial infarction and in unstable angina pectoris

Tachycardia upon swallowing. Evidence for a left atrial automatic focus.

Impact of wearable devices with feedbacks for increasing daily walking activity and physical capacities in cardiovascular patients: a meta-analysis of randomized controlled trials