How to Survive a Heart Attack When Alone: coughing and deep breathing? too little too late.

How to Survive a Heart Attack When Alone: coughing and deep breathing?
This email doing the rounds may be inappropriate advice that could cost people their lives. – see and

BUT an apparently reputable cardiologist (apparently ex Vietnam Medic) also recommends it:

BUT see the notes of caution at

In short, it may save those who have sudden arrhythmia- but it is less likely to save those who are having a huge heart attack.- for whom most interventions are too late. The compromise may be to switch on the vehicle’s emergency flicker, stop the car, start coughing while collapsing visible over the steering wheel with a hand on the hooter to attract attention..

Very very few people recover or survive well long term after spontaneous (ie non-violent, non-toxic) cardiac arrest outside hospital – the studies below from France, Germany , USA & UK indicate that successful survival without impairment is – in the best hands – below perhaps 5%. .

So only primary prevention pays. Fish oil halves sudden death; metformin halves the deathrate in type 2 diabetics – and halves new diabetes in the overweight; appropriate estrogen replacement lowers allcause premature mortality by a third; deficiency of testosterone, estradiol, minerals, vitamins, CoQ10 , arginine, carnitine and ribose play a crucial role in the development and reversibility of arrhythmia, cardio/vascular and all-cause degenerative disease; and testosterone is antiarrhythmic but estrogen arrhythmogenic.

By contrast, unlike the above proven life-extenders, no modern designer drugs for chronic use have been shown to significantly reduce all major chronic degenerative diseases and premature all-cause mortality.

Thus all should take natural supplements early and permanently – appropriate vigorous supplements of minerals, vitamins and biologicals (including fish oil, insulin sensitizers and sex hormone replacement), to minimize early vascular disease and arrhythmia potential.


Heart. 2007 ;93:601-5. Sudden arrhythmic death syndrome SADS : a national survey of sudden unexplained cardiac death.Behr ER, Casey A, Sheppard M, University of London, UK. The estimated mortality from SADS was 0.16/100 000 per annum (95% CI 0.12 to 0.21), compared with an official mortality of 0.10/100 000 per annum for International Classification of Diseases 798.1 (sudden death, cause unknown-instantaneous death) or 1.34/100 000 per annum for unascertained causes of death. CONCLUSIONS: Deaths from SADS occur predominantly in young males. When compared with official mortality, the incidence of SADS may be up to eight times higher than estimated: more than 500 potential SADS cases per annum in England. Families with SADS carry genetic cardiac disease, placing them at risk of further sudden deaths. SADS should therefore be a certifiable cause of death prompting specialised cardiological evaluation of families.

European Heart Journal 2006 27:406-412 Post-discharge survival following pre-hospital cardiopulmonary arrest due to cardiac aetiology: temporal trends and impact of changes in clinical management Jill P. Pell ea University of Glasgow,
The Heartstart Register was used to identify all 1659 patients discharged alive from Scottish hospitals during 1991–01 following pre-hospital arrest due to cardiac aetiology. Over the period studied, the proportion of people suffering pre-hospital arrest who survived to discharge from hospital changed from 11.6% (552/4766) in 1991–93, to 7.0% (558/8006) in 1997–01.

Resuscitation. 2005 65:49-55. Outcome after cardiac arrest: predictive values and limitations of the neuroproteins neuron-specific enolase and protein S-100 and the Glasgow Coma Scale. Pfeifer R, ea University of Jena, Germany.
BACKGROUND AND PURPOSE: Patients resuscitated from cardiac arrest are at risk of subsequent death or poor neurological outcome up to a persistent vegetative state. We investigated the prognostic value of several epidemiological and clinical markers in 97 patients undergoing cardiopulmonary resuscitation (CPR) after non-traumatic cardiac arrest between 1998 and 2002. RESULTS: 72.% of the patients died or remained in a persistent vegetative state; and 28.8% survived with severe, moderate or without neurological disorders. .

N Engl J Med. 1999 341(8):569-75. A comparison of standard cardiopulmonary resuscitation and active compression-decompression resuscitation for out-of-hospital cardiac arrest. French Active Compression-Decompression Cardiopulmonary Resuscitation Study Group.Plaisance P, ea .Lariboisière University Hospital, Paris, France. BACKGROUND: We previously observed that short-term survival after out-of-hospital cardiac arrest was greater with active compression-decompression cardiopulmonary resuscitation (CPR) than with standard CPR. In the current study, we assessed the effects of the active compression-decompression method on one-year survival. METHODS: Patients who had cardiac arrest in France, more than 80 percent of whom had asystole, were assigned to receive either standard CPR (377 patients) or active compression-decompression CPR (373 patients) according to whether their arrest occurred on an even or odd day of the month, respectively. The primary end point was survival at one year. The rate of survival to hospital discharge without neurologic impairment and the neurologic outcome were secondary end points. RESULTS: Both the rate of hospital discharge without neurologic impairment (6 percent vs. 2 percent, P=0.01) and the one-year survival rate (5 percent vs. 2 percent, P=0.03) were significantly higher among patients who received active compression-decompression CPR than among those who received standard CPR.

Chest. 1994 ;106:872-9. Survival after in-hospital cardiopulmonary arrest of noncritically ill patients. A prospective study. Berger R, Kelley M. Veterans Affairs Medical Center, Lexington, KY 40511.
BACKGROUND: The rising healthcare costs and the ethical and economic implications of cardiopulmonary resuscitation (CPR) have generated interest in defining criteria to predict the appropriateness of CPR in specific patients. Age has been proposed as one such a criterion. METHODS: As part of a quality assurance program, all instances of CPR (code-500) at our VA Medical Center were prospectively studied over a period of 45 months. Only events in noncritical care hospital areas were included in this analysis. The CPR data were prospectively collected, and follow-up of initial survivors was continued until the end of the study period or until a patient died. RESULTS: Of a total of 422 code-500 events, 387 (92 percent) met our study definition of cardiorespiratory arrest, and 255 of these occurred in a noncritical care area and were included in the study. Our immediate survival was 52 percent (n = 132), survival after intensive care unit (ICU) stay was 22 percent (n = 55), survival to hospital discharge was 11 percent (n = 28), and 4 percent of the patients (n = 10) were alive at the end of follow-up (mean, 22 months). None of the patients discharged alive had a significant new neurologic deficit, and all but one returned to their preadmission environment. The post-CPR hospital charges for each of the surviving patients was estimated at $63,000. Whether in-hospital CPR in noncritical care areas is cost-effective is an issue that society at large must eventually decide.

Drugs Exp Clin Res. 1992;18:355-65. Controlled study on L-carnitine therapeutic efficacy in post-infarction. Davini P, ea Santa Chiara Hospital,Pisa, Italy. A controlled study was carried out on 160 patients of both sexes (age between 39 and 86 years) discharged from the Cardiology Department of the Santa Chiara Hospital, Pisa, with a diagnosis of recent myocardial infarction. L-carnitine was randomly administered to 81 patients at an oral dose of g 4/die for 12 months, in addition to the pharmacological treatment generally used. For the whole period of 12 months, these patients showed, in comparison with the controls, an improvement in heart rate (p < 0.005), systolic arterial pressure (p < 0.005) and diastolic arterial pressure (NS); a decrease of anginal attacks (p < 0.005), of rhythm disorders (NS) and of clinical signs of impaired myocardial contractility (NS), and a clear improvement in the lipid pattern (p < 0.005). The above changes were accompanied by 90% lower mortality in the treated group (1.2%, p < 0.005), – in the control group mortality was 12.5%. Furthermore, in the control group there was a definite prevalence of deaths caused by reinfarction and sudden death. On the basis of these results, it is concluded that L-carnitine represents an effective treatment in post-infarction ischaemic cardiopathy, since it can improve the clinical evolution of this pathological condition as well as the patient’s quality of life and life expectancy.

Mol Aspects Med. 1994;15 Suppl:s165-75.
Usefulness of coenzyme Q10 in clinical cardiology: a long-term study.Langsjoen H, University of Texas Galveston .
Over an eight year period (1985-1993), we treated 424 patients with various forms of cardiovascular disease by adding coenzyme Q10 (CoQ10) to their medical regimens. Doses of CoQ10 ranged from 75 to 600 mg/day by mouth (average 242 mg). Patients were followed for an average of 17.8 months, with a total accumulation of 632 patient years. Eleven patients were omitted from this study: 10 due to non-compliance and one who experienced nausea. Eighteen deaths occurred during the study period with 10 attributable to cardiac causes.. Of 424 patients, 58 per cent improved by one NYHA class, 28% by two classes and 1.2% by three classes. A statistically significant improvement in myocardial function was documented . Before treatment with CoQ10, most patients were taking from one to five cardiac medications. During this study, overall medication requirements dropped considerably: 43% stopped between one and three drugs. Only 6% of the patients required the addition of one drug. No apparent side effects from CoQ10 treatment were noted other than a single case of transient nausea. In conclusion, CoQ10 is a safe and effective adjunctive treatment for a broad range of cardiovascular diseases, producing gratifying clinical responses while easing the medical and financial burden of multidrug therapy.

Mol Aspects Med. 1994;15 Suppl:s143-7. Coenzyme Q10 and antioxidants in acute myocardial infarction.
Kuklinski B, ea Klinikum Südstadt, Rostock, Germany.
Sixty-one patients admitted with acute myocardial infarction, and a symptom’s duration of less than 6 hr were randomized into two groups. Immediately after hospitalisation, members of the verum group (n = 32) received 500 mcg of selenium (as sodium selenite). Thereafter they received a daily dosage of 100 mg coenzyme Q10 (Bio-Quinone) and 100 mcg selenium (seleno-methionine) for a period of one year. The control group (n = 29) were given matching placebo preparations.. Biochemical parameters showed a reduced concentration of CPK- and ASAT-level in the verum group during the acute phase (although not statistically significant). None of the patients in the verum group (i.e. on antioxidative treatment) showed prolongation of the frequency corrected QT-interval. In the control group, 40% revealed a prolongation of the QT-interval by more than 440 msec (p < 0.001). There were no significant differences, with respect to early complications. During the one-year follow-up period after myocardial infarction, six patients (20%) from the control group died from re-infarction whereas one patient from the verum group suffered a non-cardiac death.

Int J Tissue React. 1990;12(3):163-8. Pronounced increase of survival of patients with cardiomyopathy when treated with coenzyme Q10 and conventional therapy. Langsjoen PH, ea Scott and White Clinic, Temple, TX USA.
During 1982-86, 43/137 patients with cardiomyopathy, Classes II, III and IV, had ejection fractions (EF) below 40%, and a mean EF of 25.1 +/- 10.3%. During treatment of these 43 patients with coenzyme Q10 (CoQ10), EF increased to 41.6 +/- 14.3% (p less than 0.001) over a mean period of 3 months (range, 2-4 months). The mean CoQ10 control blood level was 0.85 +/- 0.26 micrograms/ml which increased on treatment to 1.7 to 2.3 micrograms/ml for five periods up to 36 months (each period, p less than 0.001). The survival rates for all 137 patients treated with CoQ10 and for the 43 patients with EF below 40% were both about 75%/46 months. These two survival rates were comparable between 24 and 46 months, which is of extraordinary significance and importance when compared to survival of about 25%/36 months for 182 patients with EF below 46% on conventional therapy without CoQ10. The improved cardiac function and trippled survival show that therapy with CoQ10 is remarkably beneficial due to correction of CoQ10 deficiency in mechanisms of bioenergetics


Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Google+ photo

You are commenting using your Google+ account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )


Connecting to %s