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0 · verapamil and cocaine
1 · cocaine attack on cardiovascular system
2 · cocaine and cardiovascular system
3 · cocaine and cardiovascular disease
4 · cardiovascular effects of cocaine
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cocaine attack on cardiovascular system
Although myocardial scarring is considered a principal cause for left ventricular (LV) dysfunction in cocaine abusers, animal and human experiments showed that the administration of .Given the vascular toxicity cocaine induces, further compounded by smoking and alcohol comorbidity, and interacting with aging of the crack generation, there is a public health . A mechanism for LV dysfunction could be cocaine-induced small vessel coronary disease or direct myocardial damage 32.
Different studies performed with cardiac MRI revealed that cocaine users are characterized by ventricular dilatation and hypertrophy , associated with systolic dysfunction, .A mechanism for LV dysfunction could be cocaine-induced small vessel coronary disease or direct myocardial damage 32. In contrast, our meta-analysis on studies about asymptomatic .Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as .
This study examined left ventricular (LV) regional midwall circumferential strain by cardiac tagged magnetic resonance imaging in 32 long-term cocaine users and 14 nonusers. . Chronic cocaine use has been linked to several hallmarks of diastolic dysfunction, including increased heart weight, decreased left ventricular (LV) end-diastolic volume, and .
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The electrocardiogram is reportedly abnormal in 56 to 84 percent of patients with cocaine-related chest pain, and as many as 43 percent of cocaine abusers without myocardial .To determine the frequency and severity of clinically unrecognized left ventricular (LV) dysfunction related to cocaine use, 84 asymptomatic cocaine abusers underwent cardiac evaluation which .Given the vascular toxicity cocaine induces, further compounded by smoking and alcohol comorbidity, and interacting with aging of the crack generation, there is a public health imperative to identify pre-symptomatic markers of vascular impairments in cocaine addiction and employ preventive treatment to reduce silent disease progression.Although myocardial scarring is considered a principal cause for left ventricular (LV) dysfunction in cocaine abusers, animal and human experiments showed that the administration of intracoronary cocaine caused an acute elevation in LV pressures, LV dilation, and reduction in contractility.
A mechanism for LV dysfunction could be cocaine-induced small vessel coronary disease or direct myocardial damage 32. Different studies performed with cardiac MRI revealed that cocaine users are characterized by ventricular dilatation and hypertrophy , associated with systolic dysfunction, reduction of ejection fraction, and LV remodeling (both eccentric and concentric).A mechanism for LV dysfunction could be cocaine-induced small vessel coronary disease or direct myocardial damage 32. In contrast, our meta-analysis on studies about asymptomatic users showed that there was no significant difference in EF compared to non-users.
This study examined left ventricular (LV) regional midwall circumferential strain by cardiac tagged magnetic resonance imaging in 32 long-term cocaine users and 14 nonusers. Most of the LV segmentations in the cocaine users had less average circumferential strain in the systolic and diastolic phases.
Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis.
The electrocardiogram is reportedly abnormal in 56 to 84 percent of patients with cocaine-related chest pain, and as many as 43 percent of cocaine abusers without myocardial infarction meet.
Chronic cocaine use has been linked to several hallmarks of diastolic dysfunction, including increased heart weight, decreased left ventricular (LV) end-diastolic volume, and increased LV wall thickness. 19 Cocaine use can also impair systolic function, and compelling evidence indicates that stimulant use among already symptomatic CVD patients .
To determine the frequency and severity of clinically unrecognized left ventricular (LV) dysfunction related to cocaine use, 84 asymptomatic cocaine abusers underwent cardiac evaluation which included chest x-ray, electrocardiography (ECG), and radionuclide angiography after a two-week abstinence from cocaine use.Given the vascular toxicity cocaine induces, further compounded by smoking and alcohol comorbidity, and interacting with aging of the crack generation, there is a public health imperative to identify pre-symptomatic markers of vascular impairments in cocaine addiction and employ preventive treatment to reduce silent disease progression.Although myocardial scarring is considered a principal cause for left ventricular (LV) dysfunction in cocaine abusers, animal and human experiments showed that the administration of intracoronary cocaine caused an acute elevation in LV pressures, LV dilation, and reduction in contractility. A mechanism for LV dysfunction could be cocaine-induced small vessel coronary disease or direct myocardial damage 32.
Different studies performed with cardiac MRI revealed that cocaine users are characterized by ventricular dilatation and hypertrophy , associated with systolic dysfunction, reduction of ejection fraction, and LV remodeling (both eccentric and concentric).
A mechanism for LV dysfunction could be cocaine-induced small vessel coronary disease or direct myocardial damage 32. In contrast, our meta-analysis on studies about asymptomatic users showed that there was no significant difference in EF compared to non-users. This study examined left ventricular (LV) regional midwall circumferential strain by cardiac tagged magnetic resonance imaging in 32 long-term cocaine users and 14 nonusers. Most of the LV segmentations in the cocaine users had less average circumferential strain in the systolic and diastolic phases.Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis.
The electrocardiogram is reportedly abnormal in 56 to 84 percent of patients with cocaine-related chest pain, and as many as 43 percent of cocaine abusers without myocardial infarction meet. Chronic cocaine use has been linked to several hallmarks of diastolic dysfunction, including increased heart weight, decreased left ventricular (LV) end-diastolic volume, and increased LV wall thickness. 19 Cocaine use can also impair systolic function, and compelling evidence indicates that stimulant use among already symptomatic CVD patients .
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lv cocaine|cocaine and cardiovascular disease